15 20

CHAPTER 15
INTRACELLULAR COMPARTMENTS AND TRANSPORT
2009 Garland Science Publishing
Membrane-Enclosed Organelles
15-1
Which of the following statements about the endoplasmic reticulum (ER) is false?
(a)
The ER is the major site for new membrane synthesis in the cell.
(b)
Proteins to be delivered to the ER lumen are synthesized on smooth ER.
(c)
Steroid hormones are synthesized on the smooth ER.
(d)
The ER membrane is contiguous with the outer nuclear membrane.
15-2
Which of the following statements about membrane-enclosed organelles is true?

(a)
In a typical cell, the area of the endoplasmic reticulum membrane far exceeds the
area of plasma membrane.
(b)
The nucleus is the only organelle that is surrounded by a double membrane.
(c)
Other than the nucleus, most organelles are small and thus, in a typical cell, only
about 10% of a cells volume is occupied by membrane-enclosed organelles; the
other 90% of the cell volume is the cytosol.
(d)
The nucleus is the only organelle that contains DNA.
15-3
Name the membrane-enclosed compartments in a eucaryotic cell where each of the

functions listed below takes place.
A.
photosynthesis
B.
transcription
C.
oxidative phosphorylation
D.
modification of secreted proteins
E.
steroid hormone synthesis
F.
degradation of worn-out organelles
G.
new membrane synthesis
H.
breakdown of lipids and toxic molecules
15-4
Label the structures of the cell indicated by the lines in Figure Q15-4:
Figure Q15-4
A.
B.
C.
D.
E.
F.
G.
H.
I.
nucleus
free ribosomes
rough endoplasmic reticulum
Golgi apparatus
cytosol
endosome
plasma membrane
lysosome
mitochondrion
15-5
Which of the following organelles are not part of the endomembrane system?
(a)
Golgi apparatus
(b)
the nucleus
(c)
mitochondria
(d)
lysosomes
15-6
You discover a fungus that contains a strange star-shaped organelle not found in any other
eucaryotic cell you have seen. On further investigation you find the following.
1.
The organelle possesses a small genome in its interior.
2.
The organelle is surrounded by two membranes.
3.
Vesicles do not pinch off from the organelle membrane.
4.
The interior of the organelle contains proteins similar to those of many bacteria.
5.
The interior of the organelle contains ribosomes.
How might this organelle have arisen?
Protein Sorting
15-7
For each of the following sentences, fill in the blanks with the best word or phrase
selected from the list below. Not all words or phrases will be used; use each word or
phrase only once.
Plasma membrane proteins are inserted into the membrane in the
__________________. The address information for protein sorting in a
eucaryotic cell is contained in the __________________ of the proteins.
Proteins enter the nucleus in their __________________ form. Proteins
that remain in the cytosol do not contain a __________________. Proteins
are transported into the Golgi apparatus via __________________. The
proteins transported into the endoplasmic reticulum by
__________________ are in their __________________ form.
amino acid sequence

endoplasmic reticulum
folded
Golgi apparatus
plasma membrane
protein translocators
sorting signal
transport vesicles
unfolded
15-8
Where are proteins in the chloroplast synthesized?

(a)
in the cytosol
(b)
in the chloroplast
(c)
on the endoplasmic reticulum
(d)
in both the cytosol and the chloroplast
15-9
What would happen in each of the following cases? Assume in each case that the protein
involved is a soluble protein, not a membrane protein.
A.
You add a signal sequence (for the ER) to the N-terminal end of a normally
cytosolic protein.
B.
You change the hydrophobic amino acids in an ER signal sequence into charged
amino acids.
C.
You change the hydrophobic amino acids in an ER signal sequence into other,
hydrophobic, amino acids.
D.
You move the N-terminal ER signal sequence to the C-terminal end of the protein.
15-10 Which of the following statements is true?

(a)
The signal sequences on mitochondrial proteins are usually C-terminal.
(b)
Most mitochondrial proteins are not imported from the cytosol but are synthesized
inside the mitochondria.
(c)
Chaperone proteins in the mitochondria facilitate the movement of proteins across
the outer and inner mitochondrial membranes.
(d)
Mitochondrial proteins cross the membrane in their native, folded state.
15-11 Most proteins destined to enter the endoplasmic reticulum
(a)
are transported across the membrane after their synthesis is complete.
(b)
are synthesized on free ribosomes in the cytosol.
(c)
begin to cross the membrane while still being synthesized.
(d)
remain within the endoplasmic reticulum.
15-12 After isolating the rough endoplasmic reticulum from the rest of the cytoplasm, you
purify the RNAs attached to it. Which of the following proteins do you expect the RNA
from the rough endoplasmic reticulum to encode?
(a)
soluble secreted proteins
(b)
ER membrane proteins
(c)
plasma membrane proteins
(d)
all of the above
15-13 In which cellular location would you expect to find ribosomes translating mRNAs that
encode ribosomal proteins?
(a)
the nucleus
(b)
on the rough ER
(c)
(d)
in the cytosol
in the lumen of the ER
15-14 You are trying to identify the peroxisome-targeting sequence in the thiolase enzyme in
yeast. The thiolase enzyme normally resides in the peroxisome and therefore must
contain amino acid sequences that are used to target the enzyme for import into the
peroxisome. To identify the targeting sequences, you create a set of hybrid genes that
encode fusion proteins containing part of the thiolase protein fused to another protein,
histidinol dehydrogenase (HDH). HDH is a cytosolic enzyme required for the synthesis
of the amino acid histidine and cannot function if it is localized in the peroxisome. You
genetically engineer a series of yeast cells to express these fusion proteins instead of their
own versions of these enzymes. If the fusion proteins are imported into the peroxisome,
the HDH portion of the protein cannot function and the yeast cells cannot grow on a
medium lacking histidine. You obtain the results shown in Figure Q15-14.
Figure Q15-14
What region of the thiolase protein contains the peroxisomal targeting sequence? Explain
your answer.
15-15 What is the role of the nuclear localization sequence in a nuclear protein?
(a)
It is bound by cytoplasmic proteins that direct the nuclear protein to the nuclear
pore.
(b)
It is a hydrophobic sequence that enables the protein to enter the nuclear
membranes.
(c)
It aids in protein unfolding so that the protein can thread through nuclear pores.
(d)
It prevents the protein from diffusing out of the nucleus through nuclear pores.
15-16 A gene regulatory protein, A, contains a typical nuclear localization signal but
surprisingly is usually found in the cytosol. When the cell is exposed to hormones,
protein A moves from the cytosol into the nucleus, where it turns on genes involved in
cell division. When you purify protein A from cells that have not been treated with
hormones, you find that protein B is always complexed with it. To determine the function
of protein B, you engineer cells lacking the gene for protein B. You compare normal and
defective cells by using differential centrifugation to separate the nuclear fraction from
the cytoplasmic fraction and then separate the proteins in these fractions by gel
electrophoresis. You identify the presence of protein A and protein B by looking for their
characteristic bands on the gel. The gel you run is shown in Figure Q15-16.
Figure Q15-16
On the basis of these results, what is the function of protein B? Explain your conclusion
and propose a mechanism for how protein B works.
15-17 Your friend works in a biotechnology company and has discovered a drug that blocks the
ability of Ran to exchange GDP for GTP. What is the most likely effect of this drug on
nuclear transport?
(a)
Nuclear transport receptors would be unable to bind cargo.
(b)
Nuclear transport receptors would be unable to enter the nucleus.
(c)
Nuclear transport receptors would be unable to release their cargo in the nucleus.
(d)
Nuclear transport receptors would interact irreversibly with the nuclear pore
fibrils.
15-18 You are interested in Fuzzy, a soluble protein that functions within the ER lumen. Given
that information, which of the following statement must be true?
(a)
Fuzzy has a C-terminal signal sequence that binds to SRP.
(b)
Only one ribosome can be bound to the mRNA encoding Fuzzy during
translation.
(c)
Fuzzy must contain a hydrophobic stop-transfer sequence.
(d)
Once the signal sequence from Fuzzy has been cleaved, the signal peptide will be
ejected into the ER membrane and degraded.
15-19 Figure Q15-19 shows the organization of a protein that normally resides in the plasma
membrane. The boxes labeled 1 and 2 represent membrane-spanning sequences and the
arrow represents a site of action of signal peptidase. Given this diagram, which of the
following statements must be true?
Figure Q15-19
(a)
(b)
(c)
(d)
The N-terminus of this protein is cytoplasmic.

The C-terminus of this protein is cytoplasmic.
The mature version of this protein will span the membrane twice, with both the N
and C-termini in the cytoplasm.
None of the above.
15-20 Briefly describe the mechanism by which an internal stop-transfer sequence in a protein
causes the protein to become embedded in the lipid bilayer as a transmembrane protein
with a single membrane-spanning region. Assume that the protein has an N-terminal
signal sequence and just one internal hydrophobic stop-transfer sequence.
15-21 Using genetic engineering techniques, you have created a set of proteins that contain two
(and only two) conflicting signal sequences that specify different compartments. Predict
which signal would win out for the following combinations. Explain your answers.
A.
Signals for import into the nucleus and import into the ER.
B.
Signals for export from the nucleus and import into the mitochondria.
C.
Signals for import into mitochondria and retention in the ER.
15-22 Figure Q15-22 shows the orientation of a multipass transmembrane protein after it has
completed its entry into the ER membrane (part A) and after it gets delivered to the
plasma membrane (part B). This protein has an N-terminal signal sequence (depicted as
the dark gray membrane-spanning box), which signal peptidase cleaves off in the
endoplasmic reticulum. The other membrane-spanning domains in the protein are
represented as open boxes. Given that any hydrophobic membrane-spanning domain can
act as either a start-transfer region or a stop-transfer region, draw the final consequences
of the actions described below on the orientation of the protein in the plasma membrane.
Indicate on your drawing the extracellular space, the cytosolic face, and the plasma
membrane, as well as the N- and C-termini of the protein.
Figure Q15-22
A.
deleting the first signal sequence
B.
C.
changing the hydrophobic amino acids in the first, cleaved, sequence to charged
amino acids
changing the hydrophobic residues in every other transmembrane sequence to
charged residues, starting with the first, cleaved, signal sequence
Vesicular Transport
15-23 Which of the following choices reflects the appropriate order through which a protein
destined for the plasma membrane travels?
(a)
lysosome endosome plasma membrane
(b)
ER lysosome plasma membrane
(c)
Golgi lysosome plasma membrane
(d)
ER Golgi plasma membrane
15-24 For each of the following sentences, fill in the blanks with the best word or phrase
selected from the list below. Not all words or phrases will be used; use each word or
phrase only once.
Proteins are transported out of a cell via the __________________ or
__________________ pathway. Fluids and macromolecules are
transported into the cell via the __________________ pathway. All
proteins being transported out of the cell pass through the
__________________ and the __________________. Transport vesicles
link organelles of the __________________ system. The formation of
__________________ in the endoplasmic reticulum stabilizes protein
structure.
carbohydrate
disulfide bonds
endocytic
endomembrane
endosome
exocytic
Golgi apparatus
hydrogen bonds
ionic bonds
lysosome
protein
secretory
15-25 Which of the following statements about vesicle budding from the Golgi is false?
(a)
Clathrin molecules are important for binding to and selecting cargos for transport.
(b)
Adaptins interact with clathrin.
(c)
Once vesicle budding occurs, clathrin molecules are released from the vesicle.
(d)
Clathrin molecules act at the cytosolic surface of the Golgi membrane.
15-26 Your friend has just joined a lab that studies vesicle budding from the Golgi and has been
given a cell line that does not form mature vesicles. He wants to start designing some
experiments but wasnt listening carefully when he was told about the molecular defect of
this cell line. Hes too embarrassed to ask and comes to you for help. He does recall that
this cell line forms coated pits but vesicle budding and the removal of coat proteins dont
happen. Which of the following proteins might be lacking in this cell line?
(a)
clathrin
(b)
Rab
(c)
dynamin
(d)
adaptin
15-27 Which of the following protein families are not involved in directing transport vesicles to
the target membrane?
(a)
SNAREs
(b)
Rabs
(c)
tethering proteins
(d)
adaptins
15-28 An individual transport vesicle
(a)
contains only one type of protein in its lumen.
(b)
will fuse with only one type of membrane.
(c)
is endocytic if it is traveling toward the plasma membrane.
(d)
is enclosed by a membrane with the same lipid and protein composition as the
membrane of the donor organelle.
15-29 v-SNAREs and t-SNARES mediate the recognition of a vesicle with its target membrane
so that a vesicle displaying a particular type of v-SNARE will only fuse with a target
membrane containing a complementary type of t-SNARE. In some cases, v-SNAREs and
t-SNAREs may also mediate the fusion of identical membranes. In yeast cells, right
before the formation of a new cell, vesicles derived from the vacuole will come together
and fuse to form a new vacuole destined for the new cell. Unlike the situation we have
discussed in class, the vacuolar vesicles contain both v-SNAREs and t-SNAREs. Your
friend is trying to understand the role of these SNAREs in the formation of the new
vacuole and consults with you regarding the interpretation of his data.
Your friend has designed an ingenious assay for the fusion of vacuolar vesicles by using
alkaline phosphatase. The protein alkaline phosphatase is made in a pro form that must
be cleaved for the protein to be active. Your friend has designed two different strains of
yeast: strain A produces the pro form of alkaline phosphatase (pro-Pase), whereas strain
B produces the protease that can cleave pro-Pase into the active form (Pase). Neither
strain has the active form of the alkaline phosphatase, but when vacuolar vesicles from
the strains A and B are mixed, fusion of vesicles generates active alkaline phosphatase,
whose activity can be measured and quantified.
Figure Q15-29
Your friend has taken each of these yeast strains and further engineered them so that they
express only the v-SNAREs, only the t-SNAREs, both SNAREs (the normal situation), or
neither SNARE. He then isolates vacuolar vesicles from all strains and tests the ability of
each variant form of strain A to fuse with each variant form of strain B, by using the
alkaline phosphatase assay. The data are shown in the graph in Figure Q15-29B. On this
graph, the SNARE present on the vesicle of the particular yeast strain is indicated as v
(for the presence of the v-SNARE) and t (for the presence of the t-SNARE).
What do his data say about the requirements for v-SNAREs and t-SNAREs in the
vacuolar vesicles? Is it important to have a specific type of SNARE (that is, v-SNARE or
t-SNARE) on each vesicle?
Secretory Pathway
15-30 N-linked oligosaccharides on secreted glycoproteins are attached to
(a)
nitrogen atoms in the polypeptide backbone.
(b)
the serine or threonine in the sequence Asn-X-Ser/Thr.
(c)
the N-terminus of the protein.
(d)
the asparagine in the sequence Asn-X-Ser/Thr.
15-31 Name two types of protein modification that can occur in the ER but not in the cytosol.
15-32 Which of the following statements about disulfide bond formation is false?
(a)
Disulfide bonds do not form under reducing environments.
(b)
Disulfide bonding occurs by the oxidation of pairs of cysteine side chains on the
protein.
(c)
Disulfide bonding stabilizes the structure of proteins.
(d)
Disulfide bonds form spontaneously within the ER because the lumen of the ER is
oxidizing.
15-33 Cells have oligosaccharides displayed on their cell surface that are important for cellcell
recognition. Your friend discovered a transmembrane glycoprotein, GP1, on a pathogenic
yeast cell that is recognized by human immune cells. He decides to purify large amounts
of GP1 by expressing it in bacteria. To his purified protein he then adds a branched 14sugar oligosaccharide to the asparagine of the only Asn-X-Ser sequence found on GP1
(Figure Q15-33). Unfortunately, immune cells do not seem to recognize this synthesized
glycoprotein. Which of the following statements is a likely explanation for this problem?
Figure Q15.33
(a)
(b)
(c)
(d)
The oligosaccharide
should have been
added to the serine instead
of the
asparagine.
The oligosaccharide should have been added one sugar at a time.
The oligosaccharide needs to be further modified before it is mature.
The oligosaccharide needs a disulfide bond.
15-34 If you remove the ER-retention signal from a protein that normally resides in the ER
lumen, where do you predict the protein will ultimately end up? Explain your reasoning.
15-35 Which of the following statements about the unfolded protein response (UPR) is false?
(a)
Activation of the UPR results in the production of more ER membrane.
(b)
Activation of the UPR results in the production of more chaperone proteins.
(c)
Activation of the UPR occurs when receptors in the cytoplasm sense misfolded
proteins.
(d)
Activation of the UPR results in the cytoplasmic activation of gene regulatory
proteins.
15-36 Match the set of labels below with the numbered label lines on Figure Q15-36.
Figure Q15-36
A.
B.
C.
D.
E.
cisterna
Golgi stack
secretory
trans Golgi
cis Golgi
vesicle
network
network
15-37 A plasma membrane

protein carries an
oligosaccharide
containing mannose
(Man), galactose
(Gal), sialic acid (SA),
and Nacetylglucosamine
(GlcNAc). These
sugars are added to the
protein as it proceeds through the secretory pathway. First, a core oligosaccharide
containing Man and GlcNAc is added, followed by Gal, Man, SA, and GlcNAc in a
particular order. Each addition is catalyzed by a different transferase acting at a different
stage as the protein proceeds through the secretory pathway. You have isolated mutants
defective for each of the transferases, purified the membrane protein from each of the
mutants, and identified which sugars are present in each mutant protein. Table Q15-37
summarizes the results.
Table Q15-37
From these results, match each of the transferases (A, B, C, D) to its subcellular location
selected from the list below. (Assume that each location contains only one enzyme.)
1.
2.
3.
4.
central Golgi cisternae

cis Golgi network
ER
trans Golgi network
15-38 Which of the following statements about secretion is true?

(a)
The membrane of a secretory vesicle will fuse with the plasma membrane when it
discharges its contents to the cells exterior.
(b)
Vesicles for regulated exocytosis will not bud off the trans Golgi network until
the appropriate signal has been received from the cell.
(c)
The signal sequences of proteins destined for constitutive exocytosis ensure their
packaging into the correct vesicles.
(d)
Proteins destined for constitutive exocytosis aggregate as a result of the acidic pH

of the trans Golgi network.
15-39 For each of the following sentences, choose one of the two options enclosed in square
brackets to make a correct statement.
New plasma membrane reaches the plasma membrane by the
[regulated/constitutive] exocytosis pathway. New plasma membrane
proteins reach the plasma membrane by the [regulated/constitutive]
exocytosis pathway. Insulin is secreted from pancreatic cells by the
[regulated/constitutive] exocytosis pathway. The interior of the trans Golgi
network is [acidic/alkaline]. Proteins that are constitutively secreted
[aggregate/do not aggregate] in the trans Golgi network.
15-40 In a cell capable of regulated secretion, what are the three main classes of proteins that
must be separated before they leave the trans Golgi network?
Endocytic Pathways
15-41 You are working in a biotech company that has discovered a small-molecule drug called
H5434. H5434 binds to LDL receptors when they are bound to cholesterol. H5434
binding does not alter the conformation of the LDL receptors intracellular domain.
Interestingly, in vitro experiments demonstrate that addition of H5434 increases the
affinity of LDL for cholesterol and prevents cholesterol from dissociating from the LDL
receptor even in acidic conditions. Which of the following is a reasonable prediction of
what may happen when you add H5434 to cells?
(a)
Cytosolic cholesterol levels will remain unchanged relative to normal cells.
(b)
Cytosolic cholesterol levels will decrease relative to normal cells.
(c)
The LDL receptor will remain on the plasma membrane.
(d)
The uncoating of vesicles will not occur.
15-42 Name three possible fates for an endocytosed molecule that has reached the endosome.
selected from the list below. Not all words or phrases will be used; each word or phrase
should be used only once.
Eucaryotic cells are continually taking up materials from the extracellular
space by the process of endocytosis. One type of endocytosis is
__________________, which uses __________________ proteins to form
small vesicles containing fluids and molecules. After these vesicles have
pinched off from the plasma membrane, they will fuse with the
__________________, where materials that are taken into the vesicle are
sorted. A second type of endocytosis is __________________, which is
used to take up large vesicles that can contain microorganisms and cellular
debris. Macrophages are especially suited for this process, as they extend
__________________ (sheetlike projections of their plasma membrane) to

surround the invading microorganisms.
chaperone
cholesterol
clathrin
endosome
Golgi apparatus
mycobacterium
phagocytosis
pinocytosis
pseudopods
rough ER
SNARE
transcytosis
15-44 Fibroblast cells from patients W, X, Y, and Z, each of whom has a different inherited
defect, all contain inclusion bodies, which are lysosomes filled with undigested
material. You wish to identify the cellular basis of these defects. The possibilities are:
1.
2.
3.
a defect in one of the lysosomal hydrolases

a defect in the phosphotransferase that is required for mannose-6-phosphate
tagging of the lysosomal hydrolases
a defect in the mannose-6-phosphate receptor, which binds mannose-6-phosphatetagged lysosomal proteins in the trans Golgi network and delivers them to
lysosomes
When you incubate some of these mutant fibroblasts in a medium in which normal cells
have been grown, you find that the inclusion bodies disappear. Because of these results,
you suspect that the constitutive exocytic pathway in normal cells is secreting lysosomal
hydrolases that are being taken up by the mutant cells. (It is known that some mannose-6phosphate receptor molecules are found in the plasma membrane and can take up and
deliver lysosomal proteins via the endocytic pathway.) You incubate cells from each
patient with medium from normal cells and medium from each of the other mutant cell
cultures, and get the results summarized in Table Q15-44.
Table Q15-44
Indicate which defect (1, 2, 3) each patient (W, X, Y, Z) is most likely to have.
15-45 If a lysosome breaks, what protects the rest of the cell from lysosomal enzymes?
How We Know: Tracking Protein and Vesicle Transport
15-46 You have created a GFP fusion to a protein that is normally secreted from yeast cells.
Because you have learned about the use of temperature-sensitive mutations in yeast to
study protein and vesicle transport, you obtain three mutant yeast strains, each defective
in some aspect of the protein secretory process. Being a good scientist, you of course also
obtain a wild-type control strain. You decide to examine the fate of your GFP fusion
protein in these various yeast strains and engineer the mutant strains to express your GFP
fusion protein. However, in your excitement to do the experiment, you realize that you
did not label any of the mutant yeast strains and no longer know which strain is defective
in what process. You end up numbering your strains with the numbers 1 to 4, and then
you carry out the experiment anyway, obtaining the results shown in Figure Q15-46 (the
black dots represent your GFP fusion protein).
Figure Q15-46
Name the process that is defective in each of these strains. Remember that one of these
strains is your wild-type control.
CHAPTER 16
CELL COMMUNICATION
General Principles of Cell Signaling

16-1
Cell lines A and B both survive in tissue culture containing serum but do not
proliferate. Factor F is known to stimulate proliferation in cell line A. Cell line A
produces a receptor protein (R) that cell line B does not produce. To test the role
of receptor R, you introduce this receptor protein into cell line B, using
recombinant DNA techniques. You then test all of your various cell lines in the
presence of serum for their response to factor F, with the results summarized in
Table Q161.
Table Q16-1
Which of the following cannot be concluded from your results above?
(a)
Binding of Factor F to its receptor is required for proliferation of cell line
A.
(b)
Receptor R binds to Factor F to induce cell proliferation in cell line A.
(c)
Cell line A expresses a receptor for Factor F.
(d)
Factor F is not required for proliferation in cell line B.
16-2
For each of the following sentences, fill in the blanks with the best word or phrase
selected from the list below. Not all words or phrases will be used; each word or
phrase should be used only once.
Cells can signal to each other in various ways. A signal that must
be relayed to the entire body is most efficiently sent by
__________________ cells, which produce hormones that are
carried throughout the body through the bloodstream. On the other
hand, __________________ methods of cell signaling do not
require the release of a secreted molecule and are used for very
localized signaling events. During __________________
signaling, the signal remains in the neighborhood of the secreting
cell and thus acts as a local mediator on nearby cells. Finally,
__________________ signaling converts electrical impulses into a
chemical signal. Cells receive signals through a

__________________, which can be an integral membrane protein
or can reside inside the cell.
amplification
contact-dependent
endocrine
epithelial
G-protein
K+ channel
neuronal
paracrine
phosphorylation
receptor
target
16-3
Rank the following types of cell signaling from 1 to 4, with 1 representing the
type of signaling in which the signal molecule travels the least distance and 4 the
type of signaling in which the signal molecule travels the largest distance.
______ paracrine signaling
______ contact-dependent signaling
______ neuronal signaling
______ endocrine signaling
16-4
Explain why the signal molecules used in neuronal signaling work at a longer
range than those used in contact-dependent signaling.
16-5
Circle the phrase in each pair that is likely to occur more rapidly in response to an
extracellular signal.
A.
changes in cell secretion / increased cell division
B.
changes in protein phosphorylation / changes in proteins being synthesized
C.
changes in mRNA levels / changes in membrane potential
16-6
Receipt of extracellular signals can change cell behavior quickly (e.g., in seconds
or less) or much more slowly (e.g., in hours).
A.
What kind of molecular changes could cause quick changes in cell
behaviour?
B.
What kind of molecular changes could cause slow changes in cell
behaviour?
C.
Explain why the response you named in A results in a quick change,
whereas the response you named in B results in a slow change.
16-7
Which of the following statements is false?

(a)
Nucleotides and amino acids can act as extracellular signal molecules.
(b)
Some signal molecules can bind directly to intracellular proteins that bind
DNA and regulate gene transcription.
(c)
Some signal molecules are transmembrane proteins.
(d)
Dissolved gases such as nitric oxide (NO) can act as signal molecules, but
because they cannot interact with proteins they must act by affecting
membrane lipids.
16-8
All members of the steroid hormone receptor family __________________.

(a)
are cell-surface receptors
(b)
(c)
(d)
do not undergo conformational changes

are found only in the cytoplasm
interact with signal molecules that diffuse through the plasma membrane
16-9
Figure Q16-9
Given the generic signaling pathway in Figure Q16-9, write the number
corresponding to the item on the line next to the descriptor below.
_________
_________
_________
_________
receptor protein
effector proteins
intracellular signaling proteins
ligand
16-10 The lab you work in has discovered a previously unidentified extracellular signal
molecule called QGF, a 75,000-dalton protein. You add purified QGF to different
types of cells to determine its effect on these cells. When you add QGF to heart
muscle cells, you observe an increase in cell contraction. When you add it to
fibroblasts, they undergo cell division. When you add it to nerve cells, they die.
When you add it to glial cells, you do not see any effect on cell division or
survival. Given these observations, which of the following statements is most
likely to be true?
(a)
Because it acts on so many diverse cell types, QGF probably diffuses
across the plasma membrane into the cytoplasm of these cells.
(b)
Glial cells do not have a receptor for QGF.
(c)
(d)
QGF activates different intracellular signaling pathways in heart muscles,

fibroblasts, and nerve cells to produce the different responses observed.
Heart muscle cells, fibroblasts, and nerve cells must all have the same
receptor for GQF.
16-11 Can signaling via a steroid hormone receptor lead to amplification of the original
signal? If so, how?
16-12 Acetylcholine is a signaling molecule that elicits responses from heart muscle
cells, salivary gland cells, and skeletal muscle cells. Which of the following
statements is false?
(a)
Heart muscle cells decrease their rate and force of contraction when they
receive acetylcholine, whereas skeletal muscle cells contract.
(b)
Heart muscle cells, salivary gland cells, and skeletal muscle cells all
express an acetylcholine receptor that belongs to the transmitter-gated ion
channel family.
(c)
Active acetylcholine receptors on salivary gland cells and heart muscle
cells activate different intracellular signaling pathways.
(d)
Heart muscle cells, salivary gland cells, and skeletal muscle cells all
respond to acetylcholine within minutes of receiving the signal.
16-13 When the neurotransmitter acetylcholine is applied to skeletal muscle cells, it
binds the acetylcholine receptor and causes the muscle cells to contract.
Succinylcholine, which is a chemical analog of acetylcholine, binds to the
acetylcholine receptor on skeletal muscle cells but causes the muscle to relax; it is
therefore often used by surgeons as a muscle relaxant. Propose a model for why
succinylcholine causes muscle relaxation. What might be the mechanism to
explain the different activities of acetylcholine and succinylcholine on the
acetylcholine receptor?
16-14 The local mediator nitric oxide stimulates the intracellular enzyme guanylyl
cyclase by ________________.
(a)
activating a G-protein
(b)
activating a receptor tyrosine kinase
(c)
diffusing into cells and stimulating the cyclase directly
(d)
activating an intracellular protein kinase
16-15 Figure Q16-15 shows the pathway through which nitric oxide (NO) triggers
smooth muscle relaxation in a blood-vessel wall. Which of the following
situations would lead to relaxation of the smooth muscle cells in the absence of
acetylcholine?
Figure Q16-15
(a)
(b)
(c)
(d)
a smooth muscle cell that has a defect in guanylyl cyclase such that it
cannot bind NO
a muscle cell that has a defect in guanylyl cyclase such that it
constitutively converts GTP to cyclic GMP
a muscle cell that has cyclic GMP phosphodiesterase constitutively active
a drug that blocks an enzyme involved in the metabolic pathway from
arginine to NO
16-16 For each of the following sentences, select the best word or phrase from the list
below to fill in the blanks. Not all words or phrases will be used; each word or
An extracellular signal molecule can act to change a cells behavior
by acting through cell-surface __________________ that control
intracellular signaling proteins. These intracellular signaling
proteins ultimately change the activity of __________________
proteins that bring about cell responses. Intracellular signaling
proteins can __________________ the signal received to evoke a
strong response from just a few extracellular signal molecules. A
cell that receives more than one extracellular signal at the same
time can __________________ this information using intracellular
signaling proteins. __________________ proteins can act as
molecular switches, letting a cell know that a signal has been
received. Enzymes that phosphorylate proteins, termed
___________, can also serve as molecular switches; the actions of
these enzymes are countered by the activity of
__________________.
GMP-binding
GTP-binding
protein phosphatases
neurotransmitter
amplify
acetylase
effector
decrease
esterases
integrate
AMP-binding
receptors
cleavage
decouple
sterols
convolute
protein kinases
autocrine
16-17 Name the three main classes of cell-surface receptor.

(a)
Extracellular signal molecules that are hydrophilic must bind to a cellsurface receptor so as to signal a target cell to change its behavior.
(b)
To function, all extracellular signal molecules must be transported by their
receptor across the plasma membrane into the cytosol.
(c)
A cell-surface receptor capable of binding only one type of signal
molecule can mediate only one kind of cell response.
(d)
Any foreign substance that binds to a receptor for a normal signal
molecule will always induce the same response that is produced by that
signal molecule on the same cell type.
16-19 Which of the following statements about molecular switches is false?
(a)
Phosphatases remove the phosphate from GTP on GTP-binding proteins,
turning them off.
(b)
Protein kinases transfer the terminal phosphate from ATP onto a protein.
(c)
Serine/threonine kinases are the most common types of protein kinase.
(d)
A GTP-binding protein exchanges its bound GDP for GTP to become
activated.
16-20 Intracellular steroid hormone receptors have binding sites for a signaling molecule
and a DNA sequence. How is it that the same steroid hormone receptor, which
binds to a specific DNA sequence, can regulate different genes in different cell
types?
16-21 Your friend is studying a segment of a newly discovered virus that carries an
enhancer of gene expression that confers responsiveness to glucocorticoid (a
hormone) on genes that are linked to it. He constructs two versions of a reporter
gene: one has only a minimal promoter linked to it (which contains sites for RNA
polymerase binding); the other reporter gene has both this minimal promoter plus
the viral enhancer attached to it. The reporter gene allows him to measure the
amount of transcription that occurs from each construct. Your friend puts each of
these constructs into two different cell lines and examines the expression of the
reporter gene in each cell line, as shown in Figure Q16-21. He is puzzled by these
findings and asks for your help in interpreting them.
Figure Q16-21
A.
B.
From these data, can you tell whether both cell lines contain
glucocorticoid receptors? Why?
What might account for the difference in the transcription of the reporter
gene in cell lines 1 and 2 after introduction of the construct containing the
viral enhancer in the presence of glucocorticoid?
G-Protein-Coupled Receptors
16-22 For each of the following sentences, select the best word or phrase from the list
below to fill in the blanks. Not all words or phrases will be used; each word or
G-protein-coupled receptors (GPCRs) all have a similar structure
with __________________ transmembrane domains. When a
GPCR binds an extracellular signal, an intracellular G protein,
composed of __________________ subunits, becomes activated.
__________________ of the G-protein subunits are tethered to the
plasma membrane by short lipid tails. When unstimulated, the
subunit is bound to __________________, which is exchanged for
__________________ on stimulation. The intrinsic
__________________ activity of the subunit is important for
inactivating the G protein. __________________ inhibits this
activity of the subunit, thereby keeping the subunit in an active
state.
phosphodiesterase
GTP
seven
four
GDP
diacylglycerol
five
adenylyl cyclase
cholera toxin
AMP
three
ATPase
ATP
GTPase
Ca2+
twelve
cAMP
two
16-23 Indicate by writing yes or no whether amplification of a signal could occur at

the particular steps described below. Explain your answers.
A.
An extracellular signaling molecule binds and activates a GPCR.
B.
The activated GPCRs cause G to separate from G and G.
C.
Adenylyl cyclase produces cyclic AMP.
D.
cAMP activates protein kinase A.
E.
Protein kinase A phosphorylates target proteins.
16-24 The following happens when a cell-surface receptor activates a G protein.
(a)
The subunit exchanges its bound GDP for GTP.
(b)
The GDP bound to the subunit is phosphorylated to form bound GTP.
(c)
The subunit exchanges its bound GDP for GTP.
(d)
It activates the subunit and inactivates the complex.
16-25 Acetylcholine binds to a GPCR on heart muscle, making the heart beat more
slowly. The activated receptor stimulates a G protein, which opens a K+ channel in
the plasma membrane, as shown in Figure Q16-25. Which of the following would
enhance this effect of the acetylcholine?
Figure Q16-25
(a)
(b)
(c)
(d)
addition of a high concentration of a non-hydrolyzable analog of GTP

addition of a drug that prevents the subunit from exchanging GDP for
GTP
mutations in the acetylcholine receptor that weaken the interaction
between the receptor and acetylcholine
mutations in the acetylcholine receptor that weaken the interaction
between the receptor and the G protein
16-26 Acetylcholine acts at a GPCR on heart muscle to make the heart beat more
slowly. It does so by ultimately opening K+ channels in the plasma membrane (as
diagrammed in Figure Q16-25), which decreases the cells excitability by making
it harder to depolarize the plasma membrane.
Indicate whether each of the following conditions would increase or decrease the
effect of acetylcholine.
A.
addition of a drug that stimulates the GTPase activity of the G subunit
B.
mutations in the K+ channel that keep it closed all the time
C.
D.
E.
F.
modification of the G subunit by cholera toxin

a mutation that decreases the affinity of the complex of the G protein
for the K+ channel
a mutation in the acetylcholine receptor that prevents its localization on
the cell surface
adding acetylcholinesterase to the external environment of the cell
16-27 During the mating process, yeast cells respond to pheromones secreted by other
yeast cells. These pheromones bind GPCRs on the surface of the responding cell
and lead to the activation of G proteins inside the cell. When a wild-type yeast
cell senses the pheromone, its physiology changes in preparation for mating: the
cell stops growing until it finds a mating partner. If yeast cells do not undergo the
appropriate response after sensing a pheromone, they are considered sterile. Yeast
cells that are defective in one or more components of the G protein have
characteristic phenotypes in the absence and presence of the pheromone, which
are listed in Table 16-27.
Table Q16-27 Mating phenotypes of various strains of yeast

Which of the following models is consistent with the data from the analysis of
these mutants? Explain your answer.
(a)
activates the mating response but is inhibited when bound to .
(b)
activates the mating response but is inhibited when bound to .
(c)
The G protein is inactive; either free or free complex is capable of
activating the mating response.
(d)
The G protein is active; both free and free complex are required to
inhibit the mating response
16-28 You are interested in how cyclic-AMP-dependent protein kinase A (PKA)
functions to affect learning and memory, and you decide to study its function in
the brain. It is known that, in the cells you are studying, PKA works via a signal
transduction pathway like the one depicted in Figure Q16-28. Furthermore, it is
also known that activated PKA phosphorylates the transcriptional regulator called
Nerd that then activates transcription of the gene Brainy. Which situation
described below will lead to an increase in Brainy transcription?
Figure Q16-28
(a)
(b)
(c)
(d)
a mutation in the Nerd gene that produces a protein that cannot be

phosphorylated by PKA
a mutation in the nuclear import sequence of PKA from PPKKKRKV to
PPAAAAAV
a mutation in the gene that encodes cAMP phosphodiesterase that makes
the enzyme inactive
a mutation in the gene that encodes adenylyl cyclase that renders the
enzyme unable to interact with the subunit of the G protein
16-29 Adrenaline stimulates glycogen breakdown in skeletal muscle cells by ultimately

activating glycogen phosphorylase, the enzyme that breaks down glycogen, as
depicted in Figure Q16-29.
Figure Q16-29
Which of the following statements below is false?
(a)
A constitutively active mutant form of PKA in skeletal muscle cells would
lead to a decrease in the amount of unphosphorylated phosphorylase
kinase.
(b)
not increase the affinity of adrenaline for the adrenergic receptor.
(c)
lead to an excess in the amount of glucose available.
(d)
lead to an excess in the amount of glycogen available.
16-30 Activated protein kinase C (PKC) can lead to the modification of the membrane
lipids in the vicinity of the active PKC. Figure Q16-30 shows how G proteins can
indirectly activate PKC. You have discovered the enzyme activated by PKC that
mediates the lipid modification. You call the enzyme Rafty and demonstrate that
activated PKC directly phosphorylates Rafty, activating it to modify the plasma
membrane lipids in the vicinity of the cell where PKC is active; these lipid
modifications can be detected by dyes that bind to the modified lipids. Cells
lacking Rafty do not have these modifications, even when PKC is active. Which
of the following conditions would lead to signal-independent modification of the
membrane lipids by Rafty?
Figure Q16-30
(a)
(b)
(c)
(d)
the expression of a constitutively active phospholipase C

a mutation in the GPCR that binds the signal more tightly
a Ca2+ channel in the endoplasmic reticulum with an increased affinity for
IP3
a mutation in the gene that encodes Rafty such that the enzyme can no
longer be phosphorylated by PKC
16-31 A calmodulin-regulated kinase (CaM-kinase) is involved in spatial learning and

memory. This kinase is able to phosphorylate itself such that its kinase activity is
now independent of the intracellular concentration of Ca2+. Thus the kinase stays
active after Ca2+ levels have dropped. Mice completely lacking this CaM-kinase
have severe spatial learning defects but are otherwise normal.
A.
Each of the following mutations also leads to similar learning defects. For
each case explain why.
(1)
a mutation that prevents the kinase from binding ATP
(2)
a mutation that deletes the calmodulin-binding part of the kinase
(3)
a mutation that destroys the site of autophosphorylation
B.
What would be the effect on the activity of CaM-kinase if there were a
mutation that reduced its interaction with the protein phosphatase
responsible for inactivating the kinase?
16-32 Activated GPCRs activate G proteins by reducing the strength of binding of GDP
to the subunit of the G protein, allowing GDP to dissociate and GTP (which is
present at much higher concentrations in the cell than GDP) to bind in its place.
How would the activity of a G protein be affected by a mutation that reduces the
affinity of the subunit for GDP without significantly changing its affinity for
GTP?
16-33 When adrenaline binds to adrenergic receptors on the surface of a muscle cell, it
activates a G protein, initiating an intracellular signaling pathway in which the
activated subunit activates adenylyl cyclase, thereby increasing cAMP levels in
the cell. The cAMP molecules then activate a cAMP-dependent kinase (PKA)
that, in turn, activates enzymes that result in the breakdown of muscle glycogen,
thus lowering glycogen levels. You obtain muscle cells that are defective in
various components of the signaling pathway. Referring to Figure Q16-29,
indicate how glycogen levels would be affected in the presence of adrenaline in
the following cells. Would they be higher or lower than in normal cells treated
with adrenaline?
A.
cells that lack adenylyl cyclase
B.
cells that lack the GPCR
C.
cells that lack cAMP phosphodiesterase
D.
cells that have an subunit that cannot hydrolyze GTP but can interact
properly with the and subunits
16-34 The rod photoreceptors in the eye are extremely sensitive to light. The cells sense
light through a signal transduction cascade involving light activation of a GPCR
that activates a G protein that activates cyclic GMP phosphodiesterase. How
would you expect the addition of the following drugs to affect the light-sensing
ability of the rod cells? Explain your answers.
A.
a drug that inhibits cyclic GMP phosphodiesterase
B.
a drug that is a nonhydrolyzable analog of GTP
16-35 Match the target of the G protein with the appropriate signaling outcome.
adenylyl cyclase ________
ion channels _________
phospholipase C _________
A. cleavage of inositol phospholipids

B. increase in cAMP levels
C. changes in membrane potential
Ca2+ can trigger biological effects in cells because an unstimulated
cell has an extremely __________________ concentration of free
Ca2+ in the cytosol, compared with its concentration in the
__________________ space and in the __________________,
creating a steep electrochemical gradient. When Ca2+ enters the
cytosol, it interacts with Ca2+-responsive proteins such as
__________________, which also binds diacylglycerol, and

__________________, which activates CaM-kinases.
average
phosopholipase C
peroxisome
adenylyl cyclase
extracellular
protein kinase C
high
protein kinase A
calmodulin
nuclear
low
Ca2+
intracellular
colorful
Enzyme-Coupled Receptors
16-37 The growth factor Superchick stimulates the proliferation of cultured chicken
cells. The receptor that binds Superchick is a receptor tyrosine kinase (RTK), and
many chicken tumor cell lines have mutations in the gene that encodes this
receptor. Which of the following types of mutation would be expected to promote
uncontrolled cell proliferation?
(a)
a mutation that prevents dimerization of the receptor
(b)
a mutation that destroys the kinase activity of the receptor
(c)
a mutation that inactivates the protein tyrosine phosphatase that normally
removes the phosphates from tyrosines on the activated receptor
(d)
a mutation that prevents the binding of the normal extracellular signal to
the receptor
16-38 The growth factor RGF stimulates proliferation of cultured rat cells. The receptor
that binds RGF is a receptor tyrosine kinase called RGFR. Which of the following
types of alteration to RGF would be most likely to prevent receptor dimerization?
(a)
a mutation that increases the affinity of RGFR for RGF
(b)
a mutation that prevents RGFR from binding to RGF
(c)
changing the tyrosines that are normally phosphorylated on RGFR
dimerization to alanines
(d)
changing the tyrosines that are normally phosphorylated on RGFR
dimerization to glutamic acid
16-39 A protein kinase can act as an integrating device in signaling if it
___________________.
(a)
phosphorylates more than one substrate
(b)
catalyzes its own phosphorylation
(c)
is activated by two or more proteins in different signaling pathways
(d)
initiates a phosphorylation cascade involving two or more protein kinases
16-40 Antibodies are Y-shaped molecules that have two identical binding sites. Suppose
that you have obtained an antibody that is specific for the extracellular domain of
an RTK. When the antibody binds to the RTK, it brings together two RTK
molecules. If cells containing the RTK were exposed to the antibody, would you
expect the kinase to be activated, inactivated, or unaffected? Explain your
reasoning.
16-41 Which of the following mechanisms is not directly involved in inactivating an

activated RTK?
(a)
dephosphorylation by serine/threonine phosphatases
(b)
dephosphorylation by protein tyrosine phosphatases
(c)
removal of the RTK from the plasma membrane by endocytosis
(d)
digestion of the RTK in lysosomes
16-42 You are interested in cell size regulation and discover that signaling through an
enzyme-coupled receptor is important for the growth (enlargement) of mouse
liver cells. Activation of the receptor activates adenylyl cyclase, which ultimately
leads to the activation of PKA, which then phosphorylates a transcription factor
called TFS on threonine 42. This phosphorylation is necessary for the binding of
TFS to its specific sites on DNA, where it then activates the transcription of Sze2,
a gene that encodes a protein important for liver cell growth. You find that liver
cells lacking the receptor are 15% smaller than normal cells, whereas cells that
express a constitutively activated version of PKA are 15% larger than normal liver
cells. Given these results, predict whether you would expect the cells size to be
bigger or smaller than normal cells if cells were treated in the following fashion.
A.
You change threonine 42 on TFS to an alanine residue.
B.
You create a version of the receptor that is constitutively active.
C.
You add a drug that inhibits adenylyl cyclase.
D.
You add a drug that increases the activity of cyclic AMP
phosphodiesterase.
E.
You mutate the cAMP-binding sites in the regulatory subunits of PKA, so
that the complex binds cAMP more tightly.
16-43 Male cockroaches with mutations that strongly decrease the function of an RTK
called RTKX are oblivious to the charms of their female comrades. This particular
RTK binds to a small molecule secreted by sexually mature females. Most males
carrying loss-of-function mutations in the gene for Ras protein are also unable to
respond to females. You have just read a paper in which the authors describe how
they have screened cockroaches that are mutant in RTKX for additional mutations
that partly restore the ability of males to respond to females. These mutations
decrease the function of a protein that the authors call Z. Which of the following
types of protein could Z be? Explain your answer.
(a)
a protein that activates the Ras protein by causing Ras to exchange GDP
for GTP
(b)
a protein that stimulates hydrolysis of GTP by the Ras protein
(c)
an adaptor protein that mediates the binding of the RTKX to the Ras
protein
(d)
a transcriptional regulator required for the expression of the Ras gene
Cells signal to one another in various ways. Some use extracellular

signal molecules that are dissolved gases, such as
__________________, which can diffuse easily into cells. Others
use cytokines, which bind to cytokine receptors. Cytokine
receptors have no intrinsic enzyme activity but are associated with
cytoplasmic tyrosine kinases called __________________s, which
become activated on the binding of cytokine to its receptor and go
on to phosphorylate and activate cytoplasmic transcriptional
regulators called __________________s. Some intracellular
signaling pathways involve chains of protein kinases that
phosphorylate each other, as seen in the __________________
signaling module. Lipids can also relay signals in the cell, as we
observe when phospholipase C cleaves the sugar-phosphate head
off a lipid molecule to generate the two small messenger molecules
__________________ (which remains embedded in the plasma
membrane) and __________________ (which diffuses into the
cytosol).
cyclic GMP
diacylglycerol
IP3
JAK
MAP kinase
NO
Ras
SMAD
STAT
TGF-

(a)
MAP kinase is important for phosphorylating MAP kinase kinase.
(b)
PI 3-kinase phosphorylates a lipid in the plasma membrane.
(c)
Ras becomes activated when an RTK phosphorylates its bound GDP to
create GTP.
(d)
STAT proteins phosphorylate JAK proteins, which then enter the nucleus
and activate gene transcription.
16-46 When activated by the extracellular signal protein platelet-derived growth factor
(PDGF), the PDGF receptor phosphorylates itself on multiple tyrosines (as
indicated in Figure 16-46A by the circled Ps; the numbers next to these Ps
indicate the amino acid number of the tyrosine). These phosphorylated tyrosines
serve as docking sites for proteins that interact with the activated PDGF-receptor.
These proteins are indicated in the figure, and include the proteins A, B, C, and D.
One of the cells responses to PDGF is an increase in DNA synthesis, which can
be measured by the incorporation of radioactive thymidine into the DNA.
To determine which protein or proteins, A, B, C, or D, are responsible for the
activation of DNA synthesis, you construct mutant versions of the PDGF receptor
that retain one or more tyrosine phosphorylation sites. You express these mutant
versions in cells that do not make their own PDGF receptor. In these cells, the
various mutant versions of the PDGF receptor are expressed normally, and, in
response to PDGF binding, become phosphorylated on whichever tyrosines

remain. You measure the level of DNA synthesis in cells that express the various
mutant receptors and obtain the data shown in Figure 16-46B.
Figure Q16-46
A.
B.
C.
From these data, which, if any, of proteins A, B, C, and D are involved in

the stimulation of DNA synthesis by PDGF? Explain your answer.
Which, if any, of these proteins inhibit DNA synthesis? Explain your
answer.
Which, if any, of these proteins seem to have no detectable role in DNA
synthesis? Explain your answer.
16-47 Two protein kinases, PK1 and PK2, work sequentially in an intracellular signaling
pathway. You create cells that contain inactivating mutations in the genes that
encode either PK1 or PK2 and find that these cells no longer respond to a
particular extracellular signal. You also create cells containing a version of PK1
that is permanently active and find that the cells behave as though they are
receiving the signal even when the signal is not present. When you introduce the
permanently active version of PK1 into cells that have an inactivating mutation in
PK2, you find that these cells also behave as though they are receiving the signal
even when no signal is present.
A.
From these results, does PK1 activate PK2 or does PK2 activate PK1?
Explain your answer.
B.
You now create a permanently active version of PK2 and find that cells
containing this version behave as though they are receiving the signal even
when the signal is not present. What do you predict will happen if you
introduce the permanently active version of PK2 into cells that have an
inactivating mutation in PK1?
16-48 Akt promotes the survival of many cells. It is activated by an intracellular

signaling pathway that is triggered by an RTK that activates PI 3-kinase, as
diagrammed in Figure Q16-48.
Figure Q16-48
Which of the following statements is false?
(a)
In the presence of a survival signal, Akt localizes to the plasma membrane
by binding to PIP3.
(b)
In the absence of survival signal, Bad inhibits the cell death inhibitor
protein Bcl2.
(c)
In the presence of survival signal, the cell death inhibitory protein Bcl2 is
active.
(d)
In the absence of survival signal, Bad is phosphorylated.
16-49 The last common ancestor to plants and animals was a unicellular eucaryote.
Thus, it is thought that multicellularity and the attendant demands for cell
communication arose independently in these two lineages. This evolutionary
viewpoint accounts nicely for the vastly different mechanisms that plants and
animals use for cell communication. Fungi use signaling mechanisms and
components that are very similar to those used in animals. Which of the
phylogenetic trees shown in Figure 16-49 does this observation support?
Figure Q16-49
16-50 The ethylene response in plants involves a dimeric transmembrane receptor. When
the receptor is not bound to ethylene, the receptor binds to and activates a protein
kinase, which activates an intracellular signaling pathway that leads to the
degradation of a transcriptional regulator important for transcribing the ethylene
response genes (see Fig. Q16-50). You discover a phosphatase that is important
for ethylene signaling, and you name it PtpE. Plants lacking PtpE never turn on
ethylene-response genes, even in the presence of ethylene. You find that PtpE
dephosphorylates serine 121 on the transcriptional regulator. Furthermore, plants
lacking PtpE degrade the transcriptional regulator in the presence of ethylene.
Figure Q16-50
Which of the following statements below is inconsistent with your data?
(a)
When the transcriptional regulator is phosphorylated, it activates
transcription of the ethylene-response genes.
(b)
When the transcriptional regulator is not phosphorylated, it binds to DNA.
(c)
Activation of the protein kinase that binds to the ethylene receptor leads to
inactivation of PtpE.
(d)
Binding of ethylene to its receptor leads to the activation of PtpE.
16-51 Figure Q16-51 shows that intracellular signaling pathways can be highly
interconnected.
Figure Q16-51
From the information in Figure Q16-51, which of the following statements is
incorrect?
(a)
The GPCR and the RTK both activate phospholipase C.
(b)
Activation of either the GPCR or the RTK will lead to activation of
transcriptional regulators.
(c)
CaM-kinase is only activated when the GPCR is active and not when the
RTK is active.
(d)
Ras is activated only when the RTK is active and not when the GPCR is
active.
How We Know: Untangling Cell Signaling Pathways

16-52 Figure Q16-52 shows how normal signaling works with a Ras protein acting
downstream of an RTK. You examine a cell line with a constitutively active Ras
protein that is always signaling. Which of the following conditions will turn off
signaling in this cell line?
Figure Q16-52
(a)
(b)
(c)
(d)
addition of a drug that prevents protein X from activating Ras

addition of a drug that increases the affinity of protein Y and Ras
addition of a drug that blocks protein Y from interacting with its target
addition of a drug that increases the activity of protein Y
16-53 Your friend is studying mouse fur color and has isolated the GPCR responsible for
determining its color, as well as the extracellular signal that activates the receptor.
She finds that, on addition of the signal to pigment cells (cells that produce the
pigment determining fur color), cAMP levels rise in the cell. She starts a biotech
company, and the company isolates more components of the signaling pathway
responsible for fur color. Using transgenic mouse technology, the company
genetically engineers mice that are defective in various proteins involved in
determining fur color. The company obtains the following results.
Normal mice have beige (very light brown) fur color.
Mice lacking the extracellular signal have white fur.
Mice lacking the GPCR have white fur.
Mice lacking cAMP phosphodiesterase have dark brown fur.
Your friend has also made mice that are defective in the subunit of the G protein
in this signaling pathway. The defective subunit works normally except that,
once it binds GTP, it cannot hydrolyze GTP to GDP. What color do you predict
that the fur of these mice will be? Why?
16-54 Bacteria undergo chemotaxis toward amino acids, which usually indicates the
presence of a food source. Chemotaxis receptors bind a particular amino acid and
cause changes in the bacterial cell that induce the cell to move toward the source
of the amino acid. Four types of chemotaxis receptor that mediate responses to
different amino acids have been identified in a bacterium. The receptors are called
ChrA, ChrB, ChrC, and ChrD. Each receptor specifically senses serine, aspartate,
glutamate, or glycine, although you do not know which receptor senses which
amino acid. You have been given a wild-type bacterial strain that contains all four
receptors, as well as various mutant bacterial strains that are lacking one or more
of the receptors.
To figure out which receptor senses which amino acid, you conduct experiments
in which you fill a capillary tube with an amino acid to attract the bacteria, dip the
capillary tube into a solution containing bacteria, remove the capillary tube after 5
minutes, and count the number of bacteria in the capillary tube. Your results are
shown in Table Q16-54.
Table Q16-54 Chemotaxis in wild-type and mutant strains of bacteria

From these results, indicate which receptor is used for which amino acid.
CHAPTER 17
171
CYTOSKELETON
IdentifythecytoskeletalstructuresdepictedintheepithelialcellsshowninFigure
Q171.
FigureQ171
172
Whichofthefollowingstatementsaboutthecytoskeletonisfalse?
(a)
Thecytoskeletonismadeupofthreetypesofproteinfilament.
(b)
ThebacterialcytoskeletonisimportantforcelldivisionandDNA
segregation.
(c)
Proteinmonomersthatareheldtogetherwithcovalentbondsform
cytoskeletalfilaments.
(d)
Thecytoskeletonofacellcanchangeinresponsetotheenvironment.
173
Indicatewhichofthethreemajorclassesofcytoskeletalelementseachstatement
belowrefersto.
A.
monomerthatbindsATP
B.
includeskeratinandneurofilaments
C.
importantforformationofthecontractileringduringcytokinesis
D.
supportsandstrengthensthenuclearenvelope
E.
theirstabilityinvolvesaGTPcap
F.
usedintheeucaryoticflagellum
G.
acomponentofthemitoticspindle
H.
canbeconnectedthroughdesmosomes
I.
directlyinvolvedinmusclecontraction
J.
abundantinfilopodia
174
Whichofthefollowingstatementsaboutthecytoskeletonistrue?
(a)
Alleucaryoticcellshaveactin,microtubules,andintermediatefilaments
intheircytoplasm.
(b)
Thecytoskeletonprovidesarigidandunchangeablestructureimportant
fortheshapeofthecell.
(c)
Thethreecytoskeletalfilamentsperformdistincttasksinthecellandact
completelyindependentlyofoneanother.
(d)
Actinfilamentsandmicrotubuleshaveaninherentpolarity,withaplus
endthatgrowsmorequicklythantheminusend.
175
Rankthefollowingcytoskeletalfilamentsfromsmallesttolargestindiameter(1
=smallestindiameter,4=largest)
______intermediatefilaments
______microtubules
______actinfilament
______myofibril
Intermediate Filaments
176
Whichofthestatementsbelowaboutintermediatefilamentsisfalse?
(a)
Theycanstayintactincellstreatedwithconcentratedsaltsolutions.
(b)
Theycanbefoundinthecytoplasmandthenucleus.
(c)
Theycanbeanchoredtotheplasmamembraneatcellcelljunction.
(d)
Eachfilamentisabout10mindiameter.
177
Intermediatefilamentsaremadefromelongatedfibrousproteinsthatare
assembledintoaropelikestructure.FigureQ177showsthestructureofan
intermediatefilamentsubunit.Youareinterestedinhowintermediatefilaments
areformed,andyoucreateanintermediatefilamentsubunitwhosehelical
regionistwiceaslongasthatofanormalintermediatefilamentbyduplicatingthe
normalhelicalregionwhilekeepingaglobularheadattheNterminusanda
globulartailattheCterminus;youcallthissubunitIFd.Ifyouweretoassemble
intermediatefilamentsusingIF2dasthesubunit,whichofthefollowing
predictionsbelowdescribesthemostlikelyoutcome?
FigureQ177
(a)
(b)
(c)
(d)
178
FilamentsassembledusingIFdwillinteractwithdifferentcytoskeletal
components.
FilamentsassembledusingIFdwillformdimersthataretwiceaslongas
dimersassembledfromnormalintermediatefilaments.
SixteentetramersassembledfromIFdwillbeneededforaropelike
structuretoform.
DimersofIFdwillformbyinteractionswiththeNterminalglobular
headandtheCterminalglobulartail.
Foreachofthefollowingsentences,fillintheblankswiththebestwordorphrase
selectedfromthelistbelow.Notallwordsorphraseswillbeused;useeachword
orphraseonlyonce.
Intermediatefilamentsarefoundmainlyincellsthataresubjectto
mechanicalstress.Mutationsingenesthatdisruptintermediate
filamentscausesomerarehumandiseases.Forexample,theskin
ofpeoplewithepidermolysisbullosasimplexisverysusceptibleto
mechanicalinjury;peoplewiththisdisorderhavemutationsin
their__________________genes,theintermediatefilamentfound
inepithelialcells.Thesefilamentsareusuallyconnectedfromcell
tocellthroughjunctionscalled__________________s.Themain
filamentsfoundinmusclecellsbelongtothe
__________________family;peoplewithdisruptionsinthese
intermediatefilamentscanhavemusculardystrophy.Inthe
nervoussystem,__________________shelpstrengthenthe
extremelylongextensionsoftenpresentinnervecellaxons;
disruptionsintheseintermediatefilamentscanleadto
neurodegeneration.Peoplewhocarrymutationsinthegenefor
__________________,animportantproteinforcrosslinking
intermediatefilaments,haveadiseasethatcombinessymptomsof
epidermolysisbullosasimplex,musculardystrophy,and
neurodegeneration.
desmosome
lamin
synapse
keratin
kinase
179
neurofilament
plectin
vimentin
Matchthetypeofintermediatefilamentwithitsappropriatelocation.
lamins_________
A.nervecells
neurofilaments_________ B.epithelia
vimentins_________
C.nucleus
keratins_________
D.connectivetissue
1710 Keratins,neurofilaments,andvimentinsareallcategoriesofintermediate
filaments.Whichofthefollowingpropertiesbelowisnottrueofthesetypesof
intermediatefilaments?
(a)
Theystrengthencellsagainstmechanicalstress.
(b)
Dimersassociatebynoncovalentbondingtoformatetramer.
(c)
Theyarefoundinthecytoplasm.
(d)
Phosphorylationcausesdisassemblyduringeverymitoticcycle.
1711 Phosphorylationofnuclearlaminsregulatestheirassemblyanddisassembly
duringmitosis.Youaddadrugtocellsundergoingmitosisthatinhibitsthe
activityofanenzymethatdephosphorylatesnuclearlamins.Whatdoyoupredict
willhappentothesecells?Why?
1712 Youareinterestedinunderstandingtheregulationofnuclearlaminaassembly.To
createaninvitrosystemforstudyingthisprocessyoustartwithpartlypurified
nuclearlaminasubunitstowhichyouwilladdbackpurifiedcellularcomponents
todrivenuclearlaminaassembly.Beforeyoustartdoingexperiments,your
instructorsuggeststhatyouconsiderwhattypeofconditionswouldbemost
amenabletotheassemblyofnuclearlaminafromitsindividualsubunitsinvitro.
Whichofthefollowingconditionsdoyoupredictwouldbemostlikelyto
enhancetheassemblyofthenuclearlamina?
(a)
additionofphosphataseinhibitors
(b)
additionofATP
(c)
additionofaconcentratedsaltsolutionthatis10timestheconcentration
normallyfoundinthenucleoplasm
(d)
additionofproteinkinaseinhibitors
Microtubules
1713 Placethefollowinginorderofsize,fromthesmallesttothelargest.
A.
protofilament
B.
microtubule
C.
tubulin
D.
tubulindimer
E.
mitoticspindle
1714 InthethreecelloutlinesinFigureQ1714,indicatethearrangementofthe
microtubules,showingclearlytheirfreeandattachedends.Oneachfigure
indicatetheplusendandtheminusendforoneofthemicrotubules.
FigureQ1714
1715 Whichofthefollowingstatementsaboutmicrotubulesistrue?
(a)
Motorproteinsmoveinadirectionalfashionalongmicrotubulesbyusing
theinherentstructuralpolarityofaprotofilament.
(b)
Thecentromerenucleatesthemicrotubulesofthemitoticspindle.
(c)
Becausemicrotubulesaresubjecttodynamicinstability,theyareused
onlyfortransientstructuresinacell.
(d)
ATPhydrolysisbyatubulinheterodimerisimportantforcontrollingthe
growthofamicrotubule.
1716 Foreachofthefollowingsentences,fillintheblankswiththebestwordorphrase
orphraseonlyonce.
Microtubulesareformedfromthetubulinheterodimer,whichis
composedofthenucleotidebinding__________________protein
andthe__________________protein.Tubulindimersarestacked
togetherintoprotofilaments;__________________parallel
protofilamentsformthetubelikestructureofamicrotubule.
__________________ringsareimportantformicrotubule
nucleationandarefoundinthe__________________,whichis
usuallyfoundnearthecellsnucleusincellsthatarenot
undergoingmitosis.Amicrotubulethatisquicklygrowingwill
havea__________________capthathelpspreventthelossof
subunitsfromitsgrowingend.Stablemicrotubulesareusedin
ciliaandflagella;thesemicrotubulesarenucleatedfroma
__________________andinvolvea__________________plus
twoarrayofmicrotubules.Themotorprotein
__________________generatesthebendingmotionincilia;the
lackofthisproteincancauseKartagenerssyndromeinhumans.
basalbody
myosin
dynein
GTP
twentyone
tubulin
tubulin
UTP
thirteen
centrosome
tubulin
kinesin
ATP
nine
tubulin
four
vimentin
two
1717 ThehydrolysisofGTPtoGDPcarriedoutbytubulinmolecules
________________.
(a)
providestheenergyneededfortubulintopolymerize
(b)
occursbecausethepooloffreeGDPhasrunout
(c)
tipsthebalanceinfavorofmicrotubuleassembly
(d)
allowsthebehaviorofmicrotubulescalleddynamicinstability
1718 Themicrotubulesinacellformastructuralframeworkthatcanhaveallthe
followingfunctionsexceptwhichofthefollowing?
(a)
holdinginternalorganellessuchastheGolgiapparatusinparticular
positionsinthecell
(b)
creatinglongthincytoplasmicextensionsthatprotrudefromonesideof
thecell
(c)
strengtheningtheplasmamembrane
(d)
movingmaterialsfromoneplacetoanotherinsideacell
1719 Youarecuriousaboutthedynamicinstabilityofmicrotubulesanddecidetojoina
labthatworksonmicrotubulepolymerization.Thepeopleinthelabhelpyou
growsomemicrotubulesincultureusingconditionsthatallowyoutowatch
individualmicrotubulesunderamicroscope.Youcanseethemicrotubules
growingandshrinking,asyouexpect.Theprofessorwhorunsthelabgetsina
newpieceofequipment,averyfinelaserbeamthatcanbeusedtosever
microtubules.Sheisveryexcitedandwantstosevergrowingmicrotubulesat
theirmiddle,usingthelaserbeam.
A.
Doyoupredictthatthenewlyexposedmicrotubuleplusendswillgrowor
shrink?Explainyouranswer.
B.
Whatdoyouexpectwouldhappentothenewlyexposedplusendsifyou
weretogrowthemicrotubulesinthepresenceofananalogofGTPthat
cannotbehydrolyzed,andyouthenseveredthemicrotubulesinthe
middlewithalaserbeam?
1720 Whichofthefollowingstatementsregardingdynamicinstabilityisfalse?
(a)
Eachmicrotubulefilamentgrowsandshrinksindependentlyofits
neighbors.
(b)
TheGTPcaphelpsprotectagrowingmicrotubulefromdepolymerization.
(c)
GTPhydrolysisbythetubulindimerpromotesmicrotubuleshrinking.
(d)
Thenewlyfreedtubulindimersfromashrinkingmicrotubulecanbe
immediatelycapturedbygrowingmicrotubulesandaddedtotheirplus
end.
1721 Whichofthesituationsbelowwillenhancemicrotubuleshrinkage?
(a)
additionofadrugthatinhibitsGTPexchangeonfreetubulindimers
(b)
additionofadrugthatinhibitsGTPhydrolysisoftubulindimers
(c)
additionofadrugthatincreasestheaffinityoftubulinmoleculescarrying
GDPforothertubulinmolecules
(d)
additionofadrugthatblockstheabilityofatubulindimertobindto
tubulin
1722 ThegraphinFigureQ1722showsthetimecourseofthepolymerizationofpure
tubulininvitro.Youcanassumethatthestartingconcentrationoffreetubulinis
muchhigherthanitisincells.
FigureQ1722
A.
B.
Explainthereasonfortheinitiallagintherateofmicrotubuleformation.
WhydoesthecurveleveloutafterpointC?
1723 Whichofthefollowingstatementsaboutorganellarmovementinthecellisfalse?
(a)
(b)
(c)
(d)
Organellesundergosaltatorymovementinthecell.
Onlythemicrotubulecytoskeletonisinvolvedinorganellarmovement.
MotorproteinsinvolvedinorganellarmovementuseATPhydrolysisfor
energy.
Organellesareattachedtothetaildomainofmotorproteins.
1724 Microtubulesareimportantfortransportingcargoinnervecellaxons,as
diagrammedinFigureQ1724.Noticethatthetwotypesofcargoaretravelingin
oppositedirections.Whichofthefollowingstatementsislikelytobefalse?
FigureQ1724
(a)
(b)
(c)
(d)
Thegraycargoisattachedtodynein.
TheblackcargoandthegraycargorequireATPhydrolysisfortheir
motion.
Theblackcargomovingtowardtheaxonterminalcontainsadomainthat
specificallyinteractswiththetaildomainofaparticularkindofmotor.
Theblackcargoandthegraycargoaremovingalongmicrotubulesof
oppositepolarity.
1725 Doyouagreeordisagreewiththisstatement?Explainyouranswer.
Minusenddirectedmicrotubulemotors(likedyneins)delivertheir
cargototheperipheryofthecell,whereasplusenddirected
microtubulemotors(likekinesins)delivertheircargotothe
interiorofthecell.
1726 Whichofthefollowingstatementsiscorrect?
Kinesinsanddyneins____________________.
(a)
havetailsthatbindtothefilaments
(b)
movealongbothmicrotubulesandactinfilaments
(c)
oftenmoveinoppositedirectionstoeachother
(d)
derivetheirenergyfromGTPhydrolysis
1727 MatchthefollowinglabelstothenumberedlinesonFigureQ1727.
FigureQ1727
A.
B.
C.
D.
minusendofmicrotubule
tailofmotorprotein
cargoofmotorprotein
headofmotorprotein
WhichofthetwomotorsinFigureQ1727ismostprobablyakinesin?Explain
youranswer.
1728 Somelowervertebratessuchasfishandamphibianscancontroltheircolorby
regulatingspecializedpigmentcellscalledmelanophores.Thesecellscontain
small,pigmentedorganelles,termedmelanosomes,thatcanbedispersed
throughoutthecell,makingthecelldarker,oraggregatedinthecenterofthecell
tomakethecelllighter.Youpurifythemelanosomesfrommelanophoresthat
haveeitheraggregatedordispersedmelanosomesandfindthat:
1.
aggregatedmelanosomescopurifywithdynein;
2.
dispersedmelanosomescopurifywithkinesin.
Giventhissetofdata,proposeamechanismforhowtheaggregationanddispersal
ofmelanosomesoccur.
1729 Indicatewhethereachofthefollowingstatementsreferstoaciliarymicrotubule,
amicrotubuleofthemitoticspindle,bothtypesofmicrotubule,orneithertypeof
microtubule.
A.
Thebasalbodyistheorganizingcenter.
B.
Themonomerissequesteredbyprofilin.
C.
Itisarrangedina9+2array.
D.
Itisnucleatedatthecentrosome.
E.
Itusesdyneinmotors.
F.
Itisinvolvedinspermmotility.
G.
Itisinvolvedinmovingfluidoverthesurfaceofcells.
1730 Whichofthefollowingitemsbelowarenotimportantforflagellarmovement?
(a)
sarcoplasmicreticulum
(b)
ATP
(c)
dynein
(d)
microtubules
1731 FigureQ1731Ashowshowthemovementofdyneincausestheflagellumto
bend.Ifinsteadofthenormalsituation,thepolarityoftheadjacentdoubletof
microtubulesweretobereversed(seeFigureQ1731B)whatdoyoupredict
wouldhappen?
FigureQ1731
(a)
(b)
(c)
(d)
Nobendingwouldoccur.
BendingwouldoccurexactlyasdiagrammedinFigureQ1731A.
Bendingwouldoccur,exceptthattherightmicrotubuledoubletwould
movedownrelativetotheleftone.
Thetwomicrotubuledoubletswouldslideawayfromeachother.
1732 FigureQ1732showstwoisolatedouterdoubletmicrotubulesfromaeucaryotic
flagellumwiththeirassociateddyneinmolecules.
FigureQ1732
A.
B.
C.
SketchwhatwillhappentothisstructureifitissuppliedwithATP.
Sketchwhatwillhappentothisstructureifthelinkingproteinsare
removedanditissuppliedwithATP.
Inacompleteflagellum,whatwouldhappenifallthedyneinmolecules
wereactiveatthesametime?
Actin Filaments
1733 Whichofthefollowingstatementsaboutactinisfalse?
(a)
ATPhydrolysisdecreasesactinfilamentstability.
(b)
Actinatthecellcortexhelpsgoverntheshapeoftheplasmamembrane.
(c)
Actinfilamentsarenucleatedatthesideofexistingactinfilamentsin
lamellipodia.
(d)
Thedynamicinstabilityofactinfilamentsisimportantforcellmovement.
orphraseonlyonce.
Therearemanyactinbindingproteinsincellsthatcanbindto
actinandmodifyitsactivity.Someproteinssuchas
__________________bindtoactinmonomers,sequesteringthem
untilneededforfilamentformation.__________________
proteinsbindtotheendofactinfilaments.The
__________________proteinsareimportantfornucleationofthe
branchedactinstructurescommonlyfoundinthe
__________________ofmovingcells,whereas
__________________proteinsareimportantfortheformationof
unbranchedactinfilamentscommonlyfoundin
__________________.Proteinsbelongingtothe
__________________familyofGTPasesregulatechangesinthe
actincytoskeletoninresponsetoextracellularsignals.
capping
integrin
filopodia
Rho
severing
lamellipodia
ARP
bundling
gelsolin
cytochalasin
thymosin
formin
GAP
contracting
lamin
1735 Doyouagreeordisagreewiththefollowingstatement?Explainyouranswer.
Nucleotidehydrolysishasasimilarroleinactinpolymerizationandintubulin
polymerization.
1736 Actinbindingproteinsbindtoactinandcanmodifyitsproperties.Youpurifya
protein,Cap1,thatseemstobindandcaponeendofanactinfilament,although
youdonotknowwhetheritbindstheplusendortheminusend.Todetermine
whichendoftheactinfilamentyourproteinbindsto,youdecidetoexaminethe
effectofCap1onactinpolymerizationbymeasuringthekineticsofactinfilament
formationinthepresenceandtheabsenceofCap1protein.Youobtainthe
followingresults(seeFigureQ1736).DoyouthinkCap1bindstheplusendor
theminusendofactin?Explainyourreasoning.
FigureQ1736
1737 Inthecell,theconcentrationofactinmonomerishigherthantheconcentration
requiredforpurifiedactinmonomerstopolymerizeinvitro.Thymosinisa
proteinthatcanbindactinmonomers.Ifyouweretoaddadrugthatinhibitsthe
abilityofthymosintobindactinmonomers,whateffectwouldthishaveonactin
polymerization?Explainyouranswer.
1738 Whichofthefollowingstatementsisfalse?
(a)
Cytochalasinspreventactinpolymerization.
(b)
Actinfilamentsareusuallyexcludedfromthecellcortex.
(c)
Integrinsaretransmembraneproteinsthatcanbindtotheextracellular
matrix.
(d)
ARPscanpromotetheformationofbranchedactinfilaments.
1739 Cellmovementinvolvesthecoordinationofmanyeventsinthecell.Whichofthe
followingphenomenaarenotrequiredforcellmotility?
(a)
Myosinmediatedcontractionattherearofthemovingcell.
(b)
(c)
(d)
Integrinassociationwiththeextracellularenvironment.
Nucleationofnewactinfilaments.
ReleaseofCa2+fromthesarcoplasmicreticulum.
1740 Thefollowingproteinsareimportantforcellmovement.Matchthefollowing
proteinswiththeirfunction.
myosinII_________
A.nucleationofnewactinfilaments
ARPproteins_________ B.regulationoftheavailabilityofactinmonomers
profilin_________
C.involvementinfocalcontacts
integrins_________
D.contractingtherearofthecell
1741 FigureQ1741showstheleadingedgeofalamellipodium.Whichofthe
followingstatementsisfalse?
FigureQ1741
(a)
(b)
(c)
(d)
Nucleationofnewfilamentsnearattheleadingedgepushestheplasma
membraneforward.
ARPproteinsnucleatethebranchedactinfilamentsinthelamellipodia.
Cappingproteinsbindtotheminusendofactinfilaments.
ThereismoreATPboundactinattheleadingedgethanintheactin
filamentsawayfromtheleadingedge.
1742 YouareexaminingacelllineinwhichactivationoftheRhofamilymemberRac
promoteslamellipodiaformation.Whichofthefollowingstatementsismost
likelytobetrue?
(a)
CellscarryingaRacmutationthatmakesRacactasifitisalwaysbound
toGTPwillpolymerizemoreunbranchedactinfilamentsthannormal
cells.
(b)
CellscarryingaRacmutationthatmakesRacunabletoexchangeGDPfor
GTPwillpolymerizemoreunbranchedactinfilamentsthannormalcells.
(c)
(d)
CellscarryingaRacmutationthatmakesRacactasifitisalwaysbound
toGTPwillpolymerizemorebranchedactinfilamentsthannormalcells.
CellscarryingaRacmutationthatmakesRacunabletoexchangeGDPfor
GTPwillpolymerizemorebranchedactinfilamentsthannormalcells.
1743 Inthebuddingyeast,activationoftheGTPbindingproteinCdc42occurson
bindingofanexternalsignal(pheromone)toaGproteinlinkedreceptor.
ActivationofCdc42promotesactinpolymerization.Predictwouldhappento
actinpolymerization,incomparisonwithpheromonetreatedcells,inthe
followingcases.
A.
YouaddpheromonetoaninhibitorofGproteinlinkedreceptors.
B.
YouaddpheromonetoanonhydrolyzableanalogueofGTP.
1744 Yourfriendworksinabiotechcompanythathasjustdiscoveredadrugthat
seemstopromotelamellipodiaformationincells.Whichofthefollowing
moleculesbelowisunlikelytobeinvolvedinthepathwaythatthisdrugaffects?
(a)
Rac
(b)
ARP
(c)
actin
(d)
myosin
Muscle Contraction
1745 Whichofthefollowingstructuresshortenduringmusclecontraction?
(a)
myosinfilaments
(b)
flagella
(c)
sarcomeres
(d)
actinfilaments
1746 Whichofthefollowingconditionsbelowislikelytodecreasethelikelihoodof
skeletalmusclecontraction?
(a)
partialdepolarizationoftheTtubulemembrane,suchthattheresting
potentialisclosertozero
(b)
additionofadrugthatblocksCa2+bindingtotroponin
(c)
anincreaseintheamountofATPinthecell
(d)
amutationintropomyosinthatdecreasesitsaffinityfortheactinfilament
1747 Whichofthefollowingstatementsaboutskeletalmusclecontractionisfalse?
(a)
Whenamusclecellreceivesasignalfromthenervoussystem,voltage
gatedchannelsopenintheTtubulemembrane.
(b)
Thechangesinvoltageacrosstheplasmamembranethatoccurwhena
musclecellreceivesasignalfromthenervoussystemcauseaninfluxof
Ca2+intothesarcoplasmicreticulum,triggeringamusclecontraction.
(c)
(d)
Achangeintheconformationoftroponinleadstochangesintropomyosin
suchthatitnolongerblocksthebindingofmyosinheadstotheactin
filament.
Duringmusclecontraction,theZdiscsmoveclosertogetherasthemyosin
headswalktowardtheplusendsoftheactinfilaments.
Whenskeletalmusclereceivesasignalfromthenervoussystemto
contract,thesignalfromthemotorneurontriggerstheopeningofa
voltagesensitiveCa2+channelinthemusclecellsplasma
membrane,allowingCa2+toflowintothecell.
1749 Youisolatesomemusclefiberstoexaminewhatregulatesmusclecontraction.
WhenyoubathethemusclefibersinasolutioncontainingATPandCa2+,yousee
musclecontraction(experiment3inTableQ1749).Ca2+isnecessary,as
solutionscontainingATPaloneornothingdonotstimulatecontractionandthus
themuscleremainsinarelaxedstate(experiments1and2inTableQ1749).
Fromwhatyouknowaboutthemechanismofmusclecontraction,fillinyour
predictionsofwhetherthemusclewillbecontractedorrelaxedforexperiments4,
5,and6.Explainyouranswers.
TableQ1749
Extracredit:InwhatstatewouldthemusclebeifyouaddedCa2+butnoATP?
How We Know: Pursuing Motor Proteins

1750 Considertheinvitromotilityassayusingpurifiedkinesinandpurified
polymerizedmicrotubulesshowninFigureQ1750.Thethreepanelsareimages
takenat1secondintervals.Inthisfigure,threemicrotubuleshavebeennumbered
tomakeiteasytoidentifythem.Whichofthefollowingstatementsaboutthis
assayisfalse?
FigureQ1750
(a)
(b)
(c)
(d)
Kinesinmoleculesareattachedbytheirtailstoaglassslide.
Themicrotubulesusedinthisassaymustbepolymerizedusingconditions
thatstabilizetubuleformationorelsetheywouldundergodynamic
instability.
ATPmustbeaddedforthisassaytowork.
AdditionofthenonhydrolyzableATPanalog(AMPPNP)wouldcause
themicrotubulestomovefaster.
1751 Youareinterestedinstudyingkinesinmovements.Youthereforepreparesilica
beadsandcoatthemwithkinesinmoleculessothateachbead,onaverage,has
onlyonekinesinmoleculeattachedtoit.Youaddthesekinesincoatedbeadstoa
preparationofmicrotubulesyouhavepolymerized.Usingvideomicroscopy,you
watchthekinesinmovedownthemicrotubules.
A.
KinesinGFPhasbeenmeasuredtomovealongmicrotubulesatarateof
0.3m/sec,andsinglemoleculestudieshaverevealedthatkinesinmoves
alongmicrotubulesprogressively,witheachstepbeing8nm.Howmany
stepscanthekinesinmoleculetakein4seconds,assumingthatthekinesin
staysattachedtothemicrotubulefortheentire4seconds?
B.
Becauseeachkinesinmoleculeisthoughttotakeapproximately100steps
beforefallingoffthemicrotubule,willyouseeyoursilicabeadsdetach
fromthemicrotubuleduringyour4secondsofobservation?
C.
Whatwouldyoupredictwouldhappentothekinesincoatedsilicabeadsif
youweretoaddAMPPNP(anonhydrolyzableATPanalog)?
CHAPTER 18
THE CELL DIVISION CYCLE
Overview of the Cell Cycle

181
orphraseonlyonce.
Thefourphasesofthecellcycle,inorder,areG1,
__________________,__________________,and
__________________.AcellcontainsthemostDNAafter
__________________phaseofthecellcycle.Acellissmallestin
sizeafter__________________phaseofthecellcycle.Growth
occursin__________________,__________________,and
__________________phasesofthecellcycle.Acelldoesnot
entermitosisuntilithascompleted__________________
synthesis.
DNA
G1
G2
M
nucleotide
organelle
protein
S
182
WhatwouldbethemostobviousoutcomeofrepeatedcellcyclesconsistingofS
phaseandMphaseonly?
(a)
CellswouldnotbeabletoreplicatetheirDNA.
(b)
Themitoticspindlecouldnotassemble.
(c)
Cellswouldgetlargerandlarger.
(d)
Thecellsproducedwouldgetsmallerandsmaller.
183
Amutantyeaststrainstopsproliferatingwhenshiftedfrom25Cto37C.When
thesecellsareanalyzedatthetwodifferenttemperatures,usingamachinethat
sortscellsaccordingtotheamountofDNAtheycontain,thegraphsinFigure
Q183areobtained.
FigureQ183
Whichofthefollowingwouldnotexplaintheresultswiththemutant?
(a)
inabilitytoinitiateDNAreplication
(b)
inabilitytobeginMphase
(c)
inabilitytoactivateproteinsneededtoenterSphase
(d)
inappropriateproductionofasignalthatcausesthecellstoremaininG1
184
Whichofthefollowingeventsdoesnotusuallyoccurduringinterphase?
(a)
Cellsgrowinsize.
(b)
Thenuclearenvelopebreaksdown.
(c)
DNAisreplicated.
(d)
Thecentrosomesareduplicated.
185
Whatwouldhappentotheprogenyofacellthatproceededtomitosisandcell
divisionafterenteringSphasebuthadnotcompletedSphase?Keepinmindthat
highlycondensedchromatin,includingthecentromereregion,isreplicatedlatein
Sphase.Explainyouranswer.
186
Arethestatementsbelowtrueorfalse?Explainyouranswer.
A.
Statement1:Generally,inagivenorganism,theS,G2,andMphasesof
thecellcycletakeadefinedandstereotypedamountoftimeinmostcells.
B.
Statement2:Therefore,thecellcyclecontrolsystemoperatesprimarily
byatimingmechanism,inwhichtheentryintoonephasestartsatimerset
forsufficienttimetocompletetherequiredtasks.Afteragivenamountof
timehaselapsed,amolecularalarmtriggersmovementtothenext
phase.
187
Whichofthefollowingstatementsaboutthecellcycleisfalse?
(a)
Onceacelldecidestoenterthecellcycle,thetimefromstarttofinishis
thesameinalleucaryoticcells.
(b)
AnunfavorableenvironmentcancausecellstoarrestinG1.
(c)
AcellhasmoreDNAduringG2thanitdidinG1.
(d)
ThecleavagedivisionsthatoccurinanearlyembryohaveshortG1andG2
phases.
188
Whichofthefollowingdescriptionsisconsistentwiththebehaviorofacellthat
lacksaproteinrequiredforacheckpointmechanismthatoperatesinG2?
(a)
ThecellwouldbeunabletoenterMphase.
(b)
ThecellwouldbeunabletoenterG2.
(c)
ThecellwouldenterMphaseunderconditionswhennormalcellswould
not.
(d)
ThecellwouldpassthroughMphasemoreslowlythannormalcells.
How We Know: Discovery of Cyclins and Cdks

189
selectedfromthelistbelow.Notallwordsorphraseswillbeused;eachwordor
phraseshouldbeusedonlyonce.
Manyfeaturesof__________________cellsmakethemsuitable
forbiochemicalstudiesofthecellcyclecontrolsystem.For
example,thecellsareunusuallylargeandarearrestedina
__________________likephase.Whenthecellsaretriggeredto
resumecycling,thecelldivisionshaveespecially
__________________G1andG2phasesandoccur
__________________.StudieswithXenopuseggsidentifieda
partlypurifiedactivitycalled__________________thatdrivesa
restingXenopusoocyteintoMphase.MPFactivitywasfoundto
__________________duringthecellcycle,althoughtheamount
ofitskinasecomponent,called__________________,remained
constant.TheregulatorycomponentofMPF,called
__________________,hasa__________________effectonMPF
activityandplaysapartinregulatinginteractionswithits
__________________s.ThecomponentsofMPFare
evolutionarily__________________fromyeasttohumans,sothat
thecorrespondinghumangenesare__________________to
functioninyeast.
able
asynchronously
Cdk
conserved
cyclin
divergent
egg
fibroblast
G1
G2
hexokinase
inhibitory
long
M
maturationpromotingfactor
oscillate
PI3kinase
regulin
S
short
sperm
steady
stimulatory
substrate
synchronously
ubiquitin
unable
uniform
1810 MPFactivitywasdiscoveredwhencytoplasmfromaXenopusMphasecellwas
injectedintoXenopusoocytes,inducingtheoocytestoformamitoticspindle.Ina
controlexperiment,Xenopusinterphasecytoplasmwasinjectedintooocytesand
shownnottoinducetheformationofamitoticspindle.Whichofthefollowing
statementsisnotalegitimateconclusionfromthecontrolexperiment?
(a)
Thepiercingoftheoocytemembranebyaneedleisinsufficienttocause
mitoticspindleformation.
(b)
Anincreasedvolumeofcytoplasmisinsufficienttocausemitoticspindle
formation.
(c)
InjectionofextraRNAmoleculesisinsufficienttocausemitoticspindle
formation.
(d)
Componentsofaninterphasenucleusareinsufficienttocausemitotic
spindleformation.
1811 Whichofthefollowingisnotgooddirectevidencethatthecellcyclecontrol
systemisconservedthroughbillionsofyearsofdivergentevolution?
(a)
AyeastcelllackingCdkfunctioncanusethehumanCdktosubstitutefor
itsmissingCdkduringthecellcycle.
(b)
Theaminoacidsequencesofcyclinsinplantsaresimilartotheamino
acidsequencesofcylinsinhumans.
(c)
TheCdkproteinsinhumansshareconservedphosphorylationsiteswith
theCdkproteinsinyeast.
(d)
YeastcellshaveonlyoneCdk,whereashumanshavemanyCdks.
The Cell-Cycle Control System

1812 LevelsofCdkactivitychangeduringthecellcycle,inpart,because
________________.
(a)
theCdksphosphorylateeachother
(b)
theCdksactivatethecyclins
(c)
(d)
Cdkdegradationprecedesentryintothenextphaseofthecellcycle
cyclinlevelschangeduringthecycle
1813 Theconcentrationofmitoticcyclin(Mcyclin)________________.
(a)
risesmarkedlyduringMphase
(b)
isactivatedbyphosphorylation
(c)
fallstowardtheendofMphaseasaresultofubiquitylationand
degradation
(d)
ishighestinG1phase
1814 Youhaveisolatedastrainofmutantyeastcellsthatdividesnormallyat30Cbut
cannotenterMphaseat37C.Youhaveisolateditsmitoticcyclinandmitotic
CdkandfindthatbothproteinsareproducedandcanformanormalMCdk
complexatbothtemperatures.Whichofthefollowingtemperaturesensitive
mutationscouldnotberesponsibleforthebehaviorofthisstrainofyeast?
(a)
inactivationofaproteinkinasethatactsonthemitoticCdkkinase
(b)
inactivationofanenzymethatubiquitylatesMcyclin
(c)
inactivationofaphosphatasethatactsonthemitoticCdkkinase
(d)
adecreaseinthelevelsofatranscriptionalregulatorrequiredfor
producingsufficientamountsofMcyclin
1815 MatchthefollowinglabelstothenumberedlabellinesonFigureQ1815.
FigureQ1815
A.
B.
C.
D.
E.
F.
G.
H.
G1phase
mitoticcyclin
mitoticCdk
Sphase
Sphasecyclin
SphaseCdk
MPF
G2phase
1816 Youhaveisolatedamutantinwhichafractionofthenewcellsdiesoonaftercell
divisionandafractionofthelivingcellshaveanextracopyofoneormore
chromosomes.Whenyougrowthecellsunderconditionsinwhichtheytransitthe
cellcyclemoreslowly,thedefectdisappears,suggestingthatthemitoticspindle
andsegregationmachineryarenormal.Proposeabasisforthedefect.
1817 CellsintheG0state________________.
(a)
donotdivide
(b)
cannotreenterthecellcycle
(c)
haveenteredthisarreststatefromeitherG1orG2
(d)
haveduplicatedtheirDNA
1818 WhatisthemainmoleculardifferencebetweencellsinaG0stateandcellsthat
havesimplypausedinG1?
S Phase
1819 YoucreatecellswithaversionofCdc6thatcannotbephosphorylatedandthus
cannotbedegraded.Whichofthefollowingstatementsdescribesthelikely
consequenceofthischangeinCdc6?
(a)
CellswillenterSphaseprematurely.
(b)
CellswillbeunabletocompleteDNAsynthesis.
(c)
Theoriginrecognitioncomplex(ORC)willbeunabletobindtoDNA.
(d)
Cdc6willbeproducedinappropriatelyduringMphase.
(a)
DNAsynthesisbeginsatoriginsofreplication.
(b)
Theloadingoftheoriginrecognitioncomplexes(ORCs)istriggeredbyS
Cdk.
(c)
ThephosphorylationanddegradationofCdc6helptoensurethatDNAis
replicatedonlyonceineachcellcycle.
(d)
DNAsynthesiscanonlybeginafterprereplicativecomplexesassembles
ontheORCs.
1821 AttheendofDNAreplication,thesisterchromatidsareheldtogetherbythe
___________.
(a)
kinetochores
(b)
securins
(c)
cohesins
(d)
histones
1822 IrradiatedmammaliancellsusuallystopdividingandarrestataG1checkpoint.
Placethefollowingeventsintheorderinwhichtheyoccur.
A.
productionofp21
B.
DNAdamage
C.
inhibitionofcyclinCdkcomplexes
D.
accumulationandactivationofp53
1823 TheG1DNAdamagecheckpoint________________.
(a)
causescellstoproceedthroughSphasemorequickly
(b)
involvesthedegradationofp53
(c)
isactivatedbyerrorscausedduringDNAreplication
(d)
involvestheinhibitionofcyclinCdkcomplexesbyp21
M Phase
Thecellcycleconsistsofanalternationbetween
__________________,whichappearsasaperiodofdramatic
activityunderthemicroscope,andapreparativeperiodcalled
__________________,whichconsistsofthreephasescalled
__________________,__________________,and
__________________.DuringMphase,thenucleusdividesina
processcalled__________________,andthecytoplasmsplitsin
twoinaprocesscalled__________________.Thecellcycle
controlsystemreliesonsharpincreasesintheactivitiesof
regulatoryproteincalled__________________,or
__________________,totriggerSandMphases.Inactivationof
__________________isrequiredtoexitfromMphaseafter
chromosomesegregation.
APC
Cdks
condensation
cyclindependentkinases
cytokinesis
G1phase
G1Cdk
G2phase
interphase
intraphase
kinesins
Mphase
MCdk
meiosis
metaphase
microtubules
mitosis
myosins
Sphase
SCdk
1825 WhichofthefollowingdoesnotoccurduringMphaseinanimalcells?
(a)
growthofthecell
(b)
condensationofchromosomes
(c)
breakdownofnuclearenvelope
(d)
attachmentofchromosomestomicrotubules
(a)
(b)
(c)
(d)
MitoticCdkmustbephosphorylatedbyanactivatingkinase(Cak)before
itisactive.
PhosphorylationofmitoticCdkbytheinhibitorykinase(Wee1)makesthe
Cdkinactive,evenifitisphosphorylatedbytheactivatingkinase.
ActiveMCdkphosphorylatestheactivatingphosphatase(Cdc25)ina
positivefeedbackloop.
Theactivatingphosphatase(Cdc25)removesallphosphatesfrommitotic
CdksothatMCdkwillbeactive.
1827 Condensins________________.
(a)
aredegradedwhencellsenterMphase
(b)
assembleintocomplexesontheDNAwhenphosphorylatedbyMCdk
(c)
areinvolvedinholdingsisterchromatidstogether
(d)
bindtoDNAbeforeDNAreplicationbegins
1828 Whichofthefollowingstatementsistrue?
(a)
Themitoticspindleislargelymadeofintermediatefilaments.
(b)
Thecontractileringismadelargelyofmicrotubulesandactinfilaments.
(c)
Thecontractileringdividesthenucleusintwo.
(d)
Themitoticspindlehelpssegregatethechromosomestothetwodaughter
cells.
Mitosis
1829 WhichstageofmitosisinananimalcelldoeseachpartofFigureQ1829
represent?
FigureQ1829
1830 FigureQ1830showsalivingcellfromthelungepitheliumofanewtatdifferent
stagesinMphase.Ordertheselightmicrographsintothecorrectsequenceand
identifythestageinMphasethateachrepresents.
FigureQ1830
1831 NamethestageofMphaseinwhichthefollowingeventsoccur.Placethe
numbers18nexttotheletterheadingstoindicatethenormalorderofevents.
A.
alignmentofthechromosomesatthespindleequator
B.
attachmentofspindlemicrotubulestochromosomes
C.
breakdownofnuclearenvelope
D.
pinchingofcellintwo
E.
separationoftwocentrosomesandinitiationofmitoticspindleassembly
F.
reformationofthenuclearenvelope
G.
condensationofthechromosomes
H.
separationofsisterchromatids
1832 Theprincipalmicrotubuleorganizingcenterinanimalcellsisthe____________.
(a)
centrosome
(b)
centromere
(c)
kinetochore
(d)
cellcortex
1833 ExaminetheschematicrepresentationofcentrosomeduplicationinFigureQ18
33.ByanalogywithDNAreplication,wouldyouclassifycentrosomeduplication
asconservativeorsemiconservative?Explainyouranswer.
FigureQ1833
1834 BeforechromosomessegregateinMphase,theyandthesegregationmachinery
mustbeappropriatelyprepared.Indicatewhetherthefollowingstatementsare
trueorfalse.Iffalse,changeasinglenountomakethestatementtrue.
A.
Sisterchromatidsareheldtogetherbycondensinsfromthetimetheyarise
byDNAreplicationuntilthetimetheyseparateatanaphase.
B.
Cohesinsarerequiredtomakethechromosomesmorecompactandthus
topreventtanglingbetweendifferentchromosomes.
C.
Themitoticspindleiscomposedofactinfilamentsandmyosinfilaments.
D.
Microtubuledependentmotorproteinsandmicrotubulepolymerization
anddepolymerizationaremainlyresponsiblefortheorganizedmovements
ofchromosomesduringmitosis.
E.
Thecentromerenucleatesaradialarrayofmicrotubulescalledanaster,
anditsduplicationistriggeredbySCdk.
F.
Eachcentrosomecontainsapairofcentriolesandhundredsoftubulin
ringsthatnucleatethegrowthofmicrotubules.
1835 ThecytoskeletonofananimalcellchangesmarkedlybetweenG1andearlyM
phase(prophase)ofthecellcycle.Foreachofthefollowingsentences,choose
oneoftheoptionsenclosedinsquarebracketsthatbestdescribesthechangesto
thecytoskeletonanditscomponents.
Beforemitosis,thenumberofcentrosomesmust
[increase/decrease].Atthebeginningof[anaphase/prophase]in
animalcells,thecentrosomesseparateinaprocessdrivenpartlyby
interactionsbetweenthe[plus/minus]endsofmicrotubulesarising
fromthetwocentrosomes.Centrosomeseparationinitiatesthe
assemblyofthebipolarmitoticspindleandisassociatedwitha
sudden[increase/decrease]inthedynamicinstabilityof
microtubules.Incomparisonwithaninterphasemicrotubulearray,
amitoticastercontainsa[smaller/larger]numberof
[longer/shorter]microtubules.ExtractsfromMphasecellsexhibit
[increased/decreased/unchanged]ratesofmicrotubule
polymerizationandincreasedfrequenciesofmicrotubule
[shrinkage/growth].Thechangesinmicrotubuledynamicsare
largelydueto[enhanced/reduced]activityofmicrotubule
associatedproteinsand[increased/decreased]activityof
catastrophins.Thenewbalancebetweenpolymerizationand
depolymerizationofmicrotubulesisnecessaryforthemitotic
spindletomovethe[replicatedchromosomes/daughter
chromosomes]tothemetaphaseplate.
1836 Matcheachofthemainclassesofspindlemicrotubulesfromlist1withtheir
functionsandfeaturesfromlist2.
1837 Disassemblyofthenuclearenvelope________________.
(a)
causestheinnernuclearmembranetoseparatefromtheouternuclear
membrane
(b)
resultsintheconversionofthenuclearenvelopeintoproteinfree
membranevesicles
(c)
istriggeredbythephosphorylationofintegrins
(d)
mustoccurforkinetochoremicrotubulestoforminanimalcells
1838 Considerananimalcellthathaseightchromosomes(fourpairsofhomologous
chromosomes)inG1phase.Howmanyofeachofthefollowingstructureswillthe
cellhaveatmitoticprophase?
A.
sisterchromatids
B.
centromeres
C.
kinetochores
D.
centrosomes
E.
centrioles
1839 Whichofthefollowingstatementsaboutkinetochoresistrue?
(a)
Kinetochoresassembleontochromosomesduringlateprophase.
(b)
KinetochorescontainDNAbindingproteinsthatrecognizesequencesat
thetelomereofthechromosome.
(c)
Kinetochoreproteinsbindtothetubulinmoleculesattheminusendof
microtubules.
(d)
Kinetochoresassembleonchromosomesthatlackcentromeres.
1840 Isthefollowingstatementtrueorfalse?
Afterthenuclearenvelopebreaksdown,microtubulesgainaccess
tothechromosomesand,everysooften,arandomlyprobing
microtubulecapturesachromosomeandultimatelyconnectstothe
kinetochoretobecomeakinetochoremicrotubuleofthespindle.
1841 Afrienddeclaresthatchromosomesareheldatthemetaphaseplateby
microtubulesthatpushoneachchromosomefromoppositesides.Whichofthe
followingobservationsdoesnotsupportyourbeliefthatthemicrotubulesare
pullingonthechromosomes?
(a)
thejigglingmovementofchromosomesatthemetaphaseplate
(b)
thewayinwhichchromosomesbehavewhentheattachmentbetween
sisterchromatidsissevered
(c)
thewayinwhichchromosomesbehavewhentheattachmenttoone
kinetochoreissevered
(d)
theshapeofchromosomesastheymovetowardthespindlepolesat
anaphase
1842 Whyshoulditbethatdrugssuchascolchicinethatinhibitmicrotubule
polymerizationanddrugssuchasTaxolthatstabilizemicrotubulesbothinhibit
mitosis?
1843 Whichofthefollowingstatementsabouttheanaphasepromotingcomplex(APC)
isfalse?
(a)
ItpromotesthedegradationofproteinsthatregulateMphase.
(b)
ItinhibitsMCdkactivity.
(c)
Itiscontinuouslyactivethroughoutthecellcycle.
(d)
MCdkstimulatesitsactivity.
1844 Whichofthefollowingstatementsistrue?
(a)
AnaphaseAmustbecompletedbeforeanaphaseBcantakeplace.
(b)
IncellsinwhichanaphaseBpredominates,thespindlewillelongatemuch
lessthanincellsinwhichanaphaseAdominates.
(c)
InanaphaseA,bothkinetochoreandinterpolarmicrotubulesshorten.
(d)
InanaphaseB,microtubulesassociatedwiththecellcortexshorten.
1845 Whenintroducedintomitoticcells,whichofthefollowingisexpectedtoimpair
anaphaseBbutnotanaphaseA?
(a)
anantibodyagainstmyosin
(b)
ATPS,anonhydrolyzableATPanalogthatbindstoandinhibitsATPases
(c)
anantibodyagainstthemotorproteinsthatmovefromtheplusendof
microtubulestotheminusend
(d)
anantibodyagainstthemotorproteinsthatmovefromtheminusendof
microtubulestowardtheplusend
1846 Whichofthefollowingprecedethereformationofthenuclearenvelopeduring
Mphaseinanimalcells?
(a)
assemblyofthecontractilering
(b)
decondensationofchromosomes
(c)
reassemblyofthenuclearlamina
(d)
transcriptionofnucleargenes
1847 AcellwithnuclearlaminsthatcannotbephosphorylatedinMphasewillbe
unableto________________.
(a)
reassembleitsnuclearenvelopeattelophase
(b)
disassembleitsnuclearlaminaatprometaphase
(c)
begintoassembleamitoticspindle
(d)
condenseitschromosomesatprophase
1848 Thelengthsofmicrotubulesinvariousstagesofmitosisdependonthebalance
betweentheactivitiesofcatastrophins,whichdestabilizemicrotubules,and
microtubuleassociatedproteins(MAPs),whichstabilizethem.Ifyoucreated
cellswithanincreasednumberofcatastrophinmolecules,doyoupredictthe
lengthofthemitoticspindlewillbelonger,shorter,orunchanged,relativetothe
correspondingstageofmitosisinwildtypecells?Whatdoyoupredictforacell
withincreasednumbersofMAPs?Explainyourreasoning.
1849 Youhavediscoveredanewproteinthatregulatesmicrotubuledynamics.First,
youisolatedproteinsfromacellularextractthatboundtoatubulinaffinity
column.Youthenseparatedtheproteinsfromeachotherbyloadingthemixture
ofproteinsonanionexchangecolumn,elutingthecolumnwithincreasingsalt
concentrationandcollectingsmallfractionsofproteinastheydrippedfromthe
column.Totestwhethereachfractioncontainedmicrotubuleregulators,you
mixeditwithfluorescenttubulinandpurifiedcentrosomes,andthenanalyzedthe
reactionmicroscopicallytomeasurethesizeoftheastermicrotubulesformed.
Youfoundthatfractions8,9,and10promotedtheformationofunusuallylong
astermicrotubules.Becauseelectrophoreticseparationofthefractionsonagel
revealedaplentifulproteinwithanapparentmolecularweightof98kD,you
namedtheproteinp98.
A.
B.
C.
D.
Doesp98behavelikeaMAPoracatastrophin?
Proposetwowaysinwhichp98mightchangethedynamicbehaviorof
microtubulestoaccountfortheobservedchangeinmicrotubulelength.
Hint:Therearefoursimplepossiblemechanisms.
Videomicroscopyoffluorescenttubulininreactionswithpurified
centrosomesallowedyoutofollowthebehaviorofindividual
microtubulesovertime.Yougraphedthechangesinmicrotubulelengthin
theabsence(FigureQ1851A)andpresence(FigureQ1851B)ofp98.
Fiverepresentativemicrotubulesareshownforeachcondition.Doesp98
altertherateofmicrotubulegrowthorshrinkage?Doesp98alterthe
frequencyofcatastrophes(asuddenandrapiddeclineinmicrotubule
length)orrescues(whenamicrotubuleswitchesfromshrinkingto
growing)?Explainyouranswers.
Afterdemonstratingtheconsequencesofp98onmicrotubuledynamicsin
vitrowiththeuseofpurifiedcomponents,youwanttodeterminewhether
theproteinhasthesameeffectsinacomplexcellularextractthatnaturally
containsp98.Brieflydescribeanexperimentthatwillallowyouto
determinewhatp98normallydoesinmitoticextracts.
FigureQ1851
Cytokinesis
1850 Cytokinesisinanimalcells________________.
(a)
requiresATP
(b)
(c)
(d)
leavesasmallcircularscarofactinfilamentsontheinnersurfaceofthe
plasmamembrane
isoftenfollowedbyphosphorylationofintegrinsintheplasmamembrane
isassistedbymotorproteinsthatpullonmicrotubulesattachedtothecell
cortex
(a)
Thecleavagefurrowisapuckeringoftheplasmamembranecausedbythe
constrictionofaringoffilamentsattachedtotheplasmamembrane.
(b)
Thecleavagefurrowwillnotbegintoformintheabsenceofamitotic
spindle.
(c)
Thecleavagefurrowalwaysformsperpendiculartotheinterpolar
microtubules.
(d)
Thecleavagefurrowalwaysformsinthemiddleofthecell.
(a)
Cytokinesisinplantcellsismediatedbythemicrotubulecytoskeleton.
(b)
SmallmembranevesiclesderivedfromtheGolgiapparatusdelivernew
cellwallmaterialforthenewwallofthedividingcell.
(c)
Thephragmoplastformsfromtheremainsofinterpolarmicrotubulesof
themitoticspindle.
(d)
Motorproteinswalkingalongthecytoskeletonareimportantforthe
contractileringthatguidesformationofthenewcellwall.
1853 Whichorganellefragmentsduringmitosis?
(a)
endoplasmicreticulum
(b)
Golgiapparatus
(c)
mitochondrion
(d)
chloroplast
Control of Cell Number and Cell Size

1854 Programmedcelldeathoccurs________________.
(a)
bymeansofanintracellularsuicideprogram
(b)
rarelyandselectivelyonlyduringanimaldevelopment
(c)
onlyinunhealthyorabnormalcells
(d)
onlyduringembryonicdevelopment
1855 Apoptosisdiffersfromnecrosisinthatnecrosis________________.
(a)
requiresthereceptionofanextracellularsignal
(b)
causesDNAtofragment
(c)
causescellstoswellandburst,whereasapoptoticcellsshrinkand
condense
(d)
involvesacaspasecascade
1856 Whichofthefollowingstatementsaboutapoptosisistrue?
(a)
CellsthatconstitutivelyexpressBcl2willbemorepronetoundergo
apoptosis.
(b)
Theprodomainofprocaspasescontainsthecatalyticactivitynecessaryfor
procaspaseactivation.
(c)
BaxandBakpromoteapoptosisbybindingtoprocaspasesinthe
apoptosome.
(d)
Apoptosisispromotedbythereleaseofcytochromecintothecytosol
frommitochondria.
1857 Imaginethatyoucouldmicroinjectcytochromecintothecytosolofbothwild
typecellsandcellsthatwerelackingbothBaxandBak,whichareapoptosis
promotingmembersoftheBcl2familyofproteins.Wouldyouexpectone,both,
orneitherofthecelllinestoundergoapoptosis?Explainyourreasoning.
1858 Thenumberofcellsinanadulttissueoranimaldependsoncellproliferation.
Whatelsedoesitdependon?
1859 Whatisthecauseofthemassiveamountofprogrammedcelldeathofnervecells
(neurons)thatoccursinthedevelopingvertebratenervoussystem,andwhat
purposedoesitserve?
Thesurvival,__________________,andsizeofeachcellinan
animalarecontrolledbyextracellularsignalmoleculessecretedby
neighboringanddistantcells.Manyofthesesignalmoleculesbind
toacellsurface__________________andtriggervarious
intracellularsignalingpathways.Oneclassofsignalmolecules,
called__________________,stimulatescelldivisionbyreleasing
themolecularbrakesthatkeepcellsinthe__________________
or__________________phaseofthecellcycle.Membersofa
secondclassofsignalmoleculesarecalled__________________,
becausetheystimulatecellgrowthandanincreaseincellmass.
Thethirdclassofsignalmolecules,called__________________,
inhibits__________________byregulatingmembersofthe
__________________familyofproteins.Inadditiontosuch
stimulatoryfactors,somesignalproteinssuchas
__________________actnegativelyonothercells,inhibitingtheir
survival,growth,orproliferation.
anaphase
annihilation
apoptosis
arrestase
Bcl2
biosynthetic
cascades
caspase
Cdk
cyclin
differentiation
G0
G1
G2
growthfactors
interphase
ligand
M
mitogens
myostatin
nourishment
nutrition
phosphatases
proliferation
receptor
S
survivalfactors
transcription
1861 Ofthefollowingmutations,whicharelikelytocausecellcyclearrest?Ifyou
predictacellcyclearrest,indicatewhetherthecellwillarrestinearlyG1,lateG1,
orG2.Explainyouranswers.
A.
amutationinageneencodingacellsurfacemitogenreceptorthatmakes
thereceptoractiveevenintheabsenceofthemitogen
B.
amutationthatdestroyedthekinaseactivityofSCdk
C.
amutationthatallowedG1Cdktobeactiveindependentlyofits
phosphorylationstatus
D.
amutationthatremovedthephosphorylationsitesontheRbprotein
E.
amutationthatinhibitedtheactivityofRb
CHAPTER 19
SEX AND GENETICS

The Benefits of Sex

191
Organismsthatreproducesexually________________________.
(a)
mustbehaploid,unlikeorganismsthatreproduceasexually
(b)
canreproduceonlywithapartnerthatcarriesthesamealleles
(c)
(d)
createzygotesthataregeneticallyidenticaltoeachother
undergoasexualreproductivecyclethatinvolvesanalternationofhaploid
cellswiththegenerationofdiploidcells
192
Whichofthefollowingstatementsistrue?
(a)
Anothernameforthefertilizedeggcellisthezygote.
(b)
Diploidorganismsreproduceonlysexually.
(c)
Allsexuallyreproducingorganismsmusthavetwocopiesofevery
chromosome.
(d)
Gameteshaveonlyonechromosome.
193
Whichofthefollowingstatementsisfalse?
(a)
Asexualreproductiontypicallygivesrisetooffspringthataregenetically
identical.
(b)
Mutationsinsomaticcellsarepassedontoindividualsofthenext
generation.
(c)
Sexualreproductionallowsforawidevarietyofgenecombinations.
(d)
Gametesarespecializedsexcells.
194
Somaticcells___________________________.
(a)
arenotnecessaryforsexualreproductioninalleucaryoticorganisms
(b)
areusedtoproducegermlinecellswhenorganismsreachsexualmaturity
(c)
leavenoprogeny
(d)
donotcontainsexchromosomes
195
Whichofthefollowingstatementsaboutthebenefitsofsexualreproductionis
false?
(a)
Sexualreproductionpermitsenhancedsurvivalbecausethegametesthat
carryallelesenhancingsurvivalinharshenvironmentsareused
preferentiallyduringfertilization.
(b)
Unicellularorganismsthatcanundergosexualreproductionhavean
increasedabilitytoadapttoharshenvironments.
(c)
Sexualreproductionreshufflesgenes,whichisthoughttohelpspecies
surviveinnovelorvaryingenvironments.
(d)
Sexualreproductioncanspeedtheeliminationofdeleteriousalleles.
196
phrasemaybeusedmorethanonce.
Toreproducesexually,anorganismmustcreatehaploid
__________________cells,or__________________,from
diploidcellsviaaspecializedcelldivisioncalled
__________________.Duringmating,thefathershaploidcells,
called__________________inanimals,fusewiththemothers
haploidcells,called__________________.Cellfusionproducesa
diploidcellcalleda__________________,whichundergoesmany
roundsofcelldivisiontocreatetheentirebodyofthenew
individual.Thecellsproducedfromtheinitialfusioneventinclude
__________________cellsthatformmostofthetissuesofthe
bodyaswellasthe__________________linecellsthatgiverise
tothenextgenerationofprogeny.
allele
bivalent
eggs
gametes
germ
meiosis
mitosis
pedigree
pollen
somatic
sperm
zygote
197
Whyissexualreproductionmorebeneficialtoaspecieslivinginanunpredictable
environmentthantoonelivinginaconstantenvironment?
198
Isthefollowingstatementtrueorfalse?Explain.
Somaticcellsleavenoprogenyandthus,inanevolutionarysense,
existonlytohelpcreate,sustain,andpropagatethegermcells.
199
Sexualreproductionisalargedrainonthelimitedresourcesofanindividual.
Nonetheless,sexualreproductioniscommon.Infact,toallowsexual
reproduction,organismshaveevolvedmanyelaborateanatomicalstructures,
cellularprocesses,andchemicalsignals.Forexample,flowersexistentirelyto
furtherthegoalofsexualreproduction,andmanyplantshaveenlistedthehelpof
beesandbirdstoaidinthedisseminationoftheirgermcells.Describeonereason
whymostmulticellularorganismshaveevolvedtoreproducesexuallyinsteadof
relyingsolelyonasexualreproduction.
Meiosis and Fertilization

1910 Indicatewhethereachofthefollowingistrueformeiosis,mitosis,both,or
neither.
A.
formationofabivalent
B.
geneticallyidenticalproducts
C.
condensationofchromosomes
D.
segregationofallpaternalchromosomestoonecell
E.
involvementofDNAreplication
1911 Meiosisisahighlyspecializedcelldivisioninwhichseveraleventsoccurina
preciselydefinedorder.Pleaseorderthemeioticeventslistedbelow.
1.
lossofcohesinsnearcentromeres
2.
3.
4.
5.
6.
7.
8.
chromatidpairing
chromosomecondensation
chromosomereplication
degradationofcohesinsboundtochromosomearms
formationofchiasmata(chiasmata=pluralofchiasma)
homologpairing
alignmentofchromosomesatthemetaphaseplate
1912 Foreachofthefollowingsentences,chooseoneoftheoptionsenclosedinsquare
bracketstomakeacorrectstatement.
Startingwithasinglediploidcell,mitosisproduces[two/four]
[identical/different][haploid/diploid]cells,whereasmeiosisyields
[two/four][identical/different][haploid/diploid]cells.Thisis
accomplishedinmeiosisbecauseasingleroundofchromosome
[replication/segregation]isfollowedbytwosequentialroundsof
[replication/segregation].Mitosisismorelikemeiosis[I/II]than
meiosis[I/II].InmeiosisI,thekinetochoresonsisterchromatids
behave[independently/coordinately]andthusattachto
microtubulesfromthe[same/opposite]spindle.Thecohesin
mediatedgluebetween[chromatids/homologs]isregulated
differentlynearthecentromeresthanalongthechromosomearms.
Cohesionislostfirstatthe[centromeres/arms]toallow
segregationof[chromatids/homologs]andislostlateratthe
[centromeres/arms]totriggersegregationof
[chromatids/homologs].
1913 Intheabsenceofrecombination,howmanygeneticallydifferenttypesofgamete
cananorganismwithfivehomologouschromosomepairsproduce?
(a)
5
(b)
10
(c)
32
(d)
64
1914 Whichofthefollowingstatementsmostcorrectlydescribesmeiosis?
(a)
MeiosisinvolvestworoundsofDNAreplicationfollowedbyasinglecell
division.
(b)
MeiosisinvolvesasingleroundofDNAreplicationfollowedbyfour
successivecelldivisions.
(c)
MeiosisinvolvesfourroundsofDNAreplicationfollowedbytwo
(d)
MeiosisinvolvesasingleroundofDNAreplicationfollowedbytwo
1915 Adiploidcellcontaining32chromosomeswillmakeahaploidcellcontaining
___chromosomes.
(a)
8
(b)
16
(c)
30
(d)
64
1916 Imagineadiploidsexuallyreproducingorganism,Diploidussexualis,that
containsthreepairsofchromosomes.Thisorganismisunusualinthatno
recombinationbetweenhomologouschromosomesoccursduringmeiosis.
A.
Assumingthatthechromosomesaredistributedindependentlyduring
meiosis,howmanydifferenttypesofspermoreggcellscanasingle
individualofthisspeciesproduce?
B.
Whatisthelikelihoodthattwosiblingsofthisspecieswillbegenetically
identical?Youcanassumethatthehomologouschromosomesofeach
parentaredifferentfromoneanotherandfromtheircounterpartsinthe
otherparent.
1917 Youhavereceivedexactlyhalfofyourgeneticmaterialfromyourmother,who
receivedexactlyhalfofhergeneticmaterialfromhermother(yourgrandmother).
A.
Explainwhyitisunlikelythatyoushareexactlyonequarterofyour
geneticmaterialwithyourgrandmother,andinsteaditismoreaccurateto
saythatingeneralpeoplereceiveanaverageofonequarteroftheir
geneticendowmentfromeachgrandparent.
B.
Considerageneonchromosome3thatyoureceivedfromyour
grandmother.Isitlikelyyoureceivedanentirechromosome3fromyour
grandmother?Whyorwhynot?
C.
Whatportionofyourgeneticmaterialdoyousharewithyoursibling?
Youraunt?Yourcousin?
1918 Youexamineawormthathastwogenders:malesthatproducespermand
hermaphroditesthatproducebothspermandeggs.Thediploidadulthasfour
homologouspairsofchromosomesthatundergoverylittlerecombination.Given
achoice,thehermaphroditesprefertomatewithmales,butjusttoannoythe
worm,youpluckahermaphroditeoutofthewildandfertilizeitseggswithits
ownsperm.Assumingthatalltheresultingoffspringareviable,whatfractiondo
youexpecttobegeneticallyidenticaltotheparentworm?Assumethateach
chromosomeintheoriginalhermaphroditeisgeneticallydistinctfromits
homolog.
(a)
All
(b)
None
(c)
1/16
(d)
1/256
1919 Whichofthefollowingstatementsaboutmeiosisistrue?
(a)
Duringmeiosis,thepaternalchromosomespairwiththematernal
chromosomesbeforeliningupatthemetaphaseplate.
(b)
Unicellularorganismsthathaveahaploidstateundergomeiosisinsteadof
mitosisduringcelldivision.
(c)
Meiosisproducesfourgeneticallyidenticalcells.
(d)
Ingeneral,meiosisisfasterthanmitosis.
1920 FigureQ1920isadiagramofchromosomesduringmeiosis.
FigureQ1920
A.
B.
Onthediagram,indicatewhichlabellinescorrespondtothefollowing
items:(1)sisterchromatids,(2)homologouschromosomes,(3)bivalent,
(4)chiasma.
Onthefigure,drawassmallcircles(oooo)thecohesingluethatis
releasedinmeioticdivisionI,anddrawassmallcrosses(xxxx)the
cohesingluethatisreleasedinmeioticdivisionII.
1921 Duringrecombination________________________.
(a)
sisterchromatidsundergocrossingoverwitheachother
(b)
chiasmataholdchromosomestogether
(c)
onecrossovereventoccursforeachpairofhumanchromosomes
(d)
thesynaptonemalcomplexkeepsthesisterchromatidstogetheruntil
anaphaseII
1922 Afterthefirstmeioticcelldivision________________________.
(a)
twohaploidgametesareproduced
(b)
(c)
(d)
cellsareproducedthatcontainthesamenumberofchromosomesas
somaticcells
thenumberofchromosomeswillvarydependingonhowthepaternaland
maternalchromosomesalignatthemetaphaseplate
DNAreplicationoccurs
1923 Meiosisincludesarecombinationcheckpointthatisanalogoustothecheckpoints
incellcycleprogression.DoublestrandedbreaksintheDNAinitiate
recombinationinmeiosis.ThebrokenendofaDNAmoleculefindsthe
correspondingsequenceonahomologouschromosomeandexchangesa
chromosomalsegmentwithitshomolog,therebyrepairingthebreak.Ongoing
recombinationsendsanegativeregulatorysignalthatpreventscellsfromentering
meioticdivisionI.
A.
Mutationsinseveralgenesinactivatetherecombinationcheckpoint.What
doyoupredictwillhappenifacellproceedsthroughmeioticdivisionI
beforecompletingrecombination?
B.
Whatwillhappenifacellfailstoinitiaterecombinationandproceeds
throughmeioticdivisionI?MeioticdivisionII?
1924 Insomefungi,celldivisionduringmeiosisgivesrisetoanorderedsporesac
containingarowoffourhaploidspores,asshowninFigureQ1924A.The
positionofeachsporewithinthesacreflectsitsrelationtoitsneighbors;inother
words,sporesthatresultfromthesamemeiosisIIdivisionarepositionednextto
eachother.Younoticethatastrainofthefungusproducedbycrossingadark
coloredstrainwithalightcoloredstraingivesrisemostlytosporesacsasshown
inFigureQ1924B,withafewsporesacslikethoseinFigureQ1924C.Indicate
whetherthefollowingstatementsarecorrect.Explainyourreasoning.
FigureQ1924
A.
B.
C.
D.
E.
MeiosisIandmeiosisIIinthefungusoccurinthereverseorderfromthat
whichoccursinhumans.
RecombinationinthefunguscanoccurduringprophaseI.
RecombinationinthefunguscannotoccurduringprophaseII.
ThesporesacsinpanelCresultfromrecombinationbetweenthe
centromereandthegeneresponsibleforsporecolor.
Recombinationhasoccurredbetweenthegeneresponsibleforsporecolor
andtheendofthechromosomearm.
1925 Inmammals,therearetwosexchromosomes,XandY,whichbehavelike
homologouschromosomesduringmeiosis.NormalmaleshaveoneX
chromosomeandoneYchromosome,andnormalfemaleshavetwoX
chromosomes.MaleswithanextraYchromosome(XYY)arefoundoccasionally.
WhichofthefollowingcouldgiverisetosuchanXYYmale?Explainyour
answer.
(a)
nondisjunctioninthefirstmeioticdivisionofspermatogenesis;normal
meiosisinthemother
(b)
nondisjunctioninthesecondmeioticdivisionofspermatogenesis;normal
meiosisinthemother
(c)
nondisjunctioninthefirstmeioticdivisionofoogenesis;normalmeiosisin
thefather
(d)
nondisjunctioninthesecondmeioticdivisionofoogenesis;normal
meiosisinthefather
1926 Whichofthefollowingwouldnotleadtoaneuploidyduringmeiosis?
(a)
sisterchromatidssegregatinginappropriately
(b)
nonsisterchromatidssegregatinginappropriately
(c)
areciprocalrearrangementofpartsbetweennonhomologous
chromosomes(e.g.,theleftarmofchromosome2exchangingplaceswith
therightarmofchromosome3)
(d)
anextrasetofchromosomesproducedduringSphase(e.g.,ifpaternal
chromosome3werereplicatedtwice)
1927 Asinglenondisjunctioneventduringmeiosis___________________.
(a)
willblockrecombination
(b)
willoccuronlyduringmeiosisII
(c)
cannotoccurwithsexchromosomes
(d)
willinvolvetheproductionoftwonormalgametesifitoccursduring
meiosisII
1928 Duringfertilizationinhumans,_______________________.
(a)
awaveofCa2+ionsisreleasedinthefertilizedeggscytoplasm
(b)
onlyonespermbindstotheunfertilizedegg
(c)
(d)
aspermmovesinarandomfashionuntilitencountersanegg
severalspermpronucleicompeteinthecytoplasmtofusewiththeegg
nucleus
Ifadiploidorganismhas16chromosomes(andthus8pairsof
homologouschromosomes),thatorganismcanproduceonly28
geneticallydifferentgametes.
Mendel and the Laws of Inheritance

1930 WhichofthefollowingstatementsaboutMendelsexperimentsisfalse?
(a)
Thepeaplantscouldundergobothcrossfertilizationandselffertilization.
(b)
ThetruebreedingstrainswerehomozygousforthetraitsthatMendel
examined.
(c)
Theeggcancarryeithertheallelefromthematernalorthepaternal
chromosome.
(d)
AlltraitsthatMendelstudiedwererecessive.
Questions1931to1934usethefollowinginformationandFigureQ1931.These
questionsmaybeusedindependently,orasagroup.
FigureQ1931diagramsoneofMendelsexperimentsusingtheroundandwrinkledseed
traits.
FigureQ1931
1931 Whichofthefollowingcouldbeconsideredatruebreedingstrainfortheseed
shapephenotype?(SeeFigureQ1931.)
(a)
alloftheroundseededplantsproducedintheF2generation
(b)
allofthewrinkleseededplantsproducedintheF2generation
(c)
alloftheroundseededplantsproducedintheF1generation
(d)
halfoftheroundseededplantsproducedintheF2generation
1932 IfyoucrossedtheroundseededplantsobtainedintheF1generationwithatrue
breedingstrainofroundseededplants,howmanywrinkleseededplantswould
youexpecttoobtaininthenextgeneration?(SeeFigureQ1931.)
(a)
none
(b)
25%
(c)
75%
(d)
all
1933 IfyoucrossedtheroundseededplantsobtainedintheF1generationwithatrue
breedingstrainofwrinkleseededplants,howmanyroundseededplantswould
youexpecttoobtaininthenextgeneration?(SeeFigureQ1931.)
(a)
25%
(b)
50%
(c)
75%
(d)
100%
1934 Whichofthefollowingstatementsabouttheroundseededpeaplantsobtainedin
theF2generationisfalse?(SeeFigureQ1931.)
(a)
Theseplantsarephenotypicallyidenticalforseedshape.
(b)
Twothirdsoftheseplantsareexpectedtobeheterozygousfortheseed
shapeallele.
(c)
Weexpect25%oftheseplantstobehomozygousfortheseedshape
allele.
(d)
Iftheseplantswerecrossedtowrinkleseededplants,someoftheseplants
wouldproduceonlyroundseededplants.
1935 WhichofthefollowingreasonswasessentialforMendeltodisprovethetheoryof
blendedinheritance?
(a)
ThetraitsthatMendelexaminedallinvolvedgenesthatdidnotdisplay
linkage.
(b)
ThetraitsthatMendelexaminedallinvolvedthereproductivestructuresof
thepeaplant.
(c)
Mendelpioneeredtechniquespermittingthefusionofmaleandfemale
gametesfromthesameplanttoproduceazygote.
(d)
ThetraitsthatMendelexaminedinvolvedanallelethatwasdominantand
anallelethatwasrecessive.
1936 WhichofthefollowingreasonswasessentialforMendelslawofindependent
assortment?
(a)
AllthetraitsthatMendelexaminedinvolvedgenesthatdidnotdisplay
linkage.
(b)
SeveralofthephenotypesthatMendelexaminedinvolvedcolor.
(c)
Mendelobservedchromosomalsegregationinpeaplantcells.
(d)
Mendelcarriedouthisexperimentsonplantsandnotonfungi.
1937 Isthefollowingstatementtrueorfalse?Explain.
Thephenotypeofanorganismreflectsalloftheallelescarriedby
thatindividual.
1938 WithrespecttogeneEonthechromosomedrawninFigureQ1938,whichgene
isleastlikelytobehaveaccordingtoMendelslawofindependentassortment?
Explainyouranswer.
FigureQ1938
1939 Cysticfibrosisresultsfrommutationsinasinglegenethatliesonchromosome7.
Onlyhomozygousmutant(ff)individualsaresick;homozygouswildtype(FF)
andheterozygous(Ff)individualsarehealthy.Ahealthymarriedcouplehasone
childwithcysticfibrosisandthewifeispregnantwithasecondchild.
A.
Whatisthegenotypeofthemother?Thefather?
B.
Whatisthechancethatthesecondchildwillhavecysticfibrosis?
1940 Sicklecellanemiaiscausedbyamutantalleleofahemoglobingene.Individuals
withtwomutantalleleshavesicklecellanemia.Individualshomozygousand
heterozygousforthemutantgenearemoreresistanttomalariathanthosewith
twowildtypealleles.Isthismutationdominant,recessive,orcodominant?
1941 YourfriendhasobtainedsomepeaseedsfromtheAbbeyofSt.ThomasinBrno,
whereGregorMendelworked.Heisveryexcitedbecausenotonlydidheobtain
someyellowandgreenpeaseedsfromtruebreedingplants(liketheonesusedin
Mendelsfamousexperiment),hewasalsoabletoobtainsomepurplepeaseeds
fromatruebreedingplant.First,yourfriendtakesthetruebreedingyellowand
greenpeaseeds,repeatsthecrossthatGregorMendeldid,andobtainsthesame
results:hesees100%yellowseededpeaplantsintheF1generation,and75%
yellowseededpeaplantsand25%greenseededpeaplantsintheF2generation.
HisresultsareillustratedinFigureQ1941A.Yourfriendthendecidestosetup
twomorecrosses.Forcross#2,hecrossesthetruebreedingpurpleseededpea
plantstothetruebreedingyellowseededpeaplants.Theresultsfromthiscross
areshowninFigureQ1941B.Next,forcross#3,hecrossesthetruebreeding
purpleseededpeaplantstothetruebreedinggreenseededpeaplants.These
resultsareshowninFigureQ1941C.
FigureQ1941
Giventheseresults,ifyouweretotakethepurpleseededpeaplantsproducedin
theF1generationincross#2andcrossthemtothepurpleseededpeaplants
producedintheF1generationofcross#3,whatdoyouexpectthatthephenotype
oftheprogenywouldlooklike?Explainyouranswer.
1942 Youaregiventwotruebreedingstrainsofhamster.Onestrainhaswhitefurcolor
andtheotherhasadarkbrownfurcolor.Whenyoucrossthewhitefurstrainto
thedarkbrownfurstrain,youobtainF1progenythathavealightbrownfurcolor.
WhenyoucrosstheF1progenywitheachother,25%oftheF2generationhave
whitefur,25%havedarkbrownfur,and50%havelightbrownfur.Howmany
genescrucialforfurcolorationdifferbetweenthetwostartingstrains?Explain
youranswer.
Extracredit:Proposeamolecularmechanismforhowfurcolorisdeterminedin
thisspeciesofhamster.
1943 Lossoffunctionmutations________________________.
(a)
causetheproductionofproteinsthatareactiveininappropriate
circumstances
(b)
willusuallyshowaphenotypewhenheterozygous
(c)
areonlypresentinapopulationatbarelydetectablelevels
(d)
areusuallyrecessive
Genetics as an Experimental Tool

1944 Conditionalallelesaremutantgeneversionsencodingproteinsthatcanfunction
normallyatthepermissiveconditionbutaredefectiveattherestrictivecondition.
Onecommonlyusedconditionistemperature.Conditionalallelesareespecially
usefultogeneticistsbecausetheypermitthestudyofessentialgenes.Atthe
permissivetemperature,theorganismlivesnormally.Whentheorganismis
shiftedtothenonpermissivetemperature,theeffectofinactivatingthegenecan
bestudied.WhichofthethreetypesofmutationshowninFigureQ1944ismost
likelytoleadtoaconditionalallele?Explainyouranswer.
FigureQ1944
1945 YouperformedageneticscreeninC.elegansandfoundtwomutations(#1and
#2)thatcauseantisocialbehavior.Youwanttolearnwhetherthesearemutations
inthesamegeneordifferentgenes,soyoucrossmutant#1andmutant#2
togethertoperformacomplementationtest.Imaginethatthemutationsarein
differentgenes:mutation#1isingeneMandmutation#2ingeneN.
FigureQ1945
A.
B.
C.
D.
Whatistheoutcomeofacomplementationtestif#1and#2areboth
recessivemutations(mandn,respectively)?Fillintheemptyovalin
FigureQ1945Aandindicatewhethertheoffspringexhibitssocialor
antisocialbehavior.
Whatistheoutcomeif#1isdominantand#2isrecessive(M*andn)?Fill
intheemptyovalinFigureQ1945Bandindicatewhethertheoffspring
exhibitssocialorantisocialbehavior.
ForthecaseinA,wouldthephenotypeoftheoffspringdifferifthetwo
mutationswereinthesamegene?
ForthecaseinB,wouldthephenotypeoftheoffspringdifferifthetwo
mutationswereinthesamegene?Arecomplementationtestsusefulfor
analyzingdominantmutations?
Atraitthatisfoundatalowfrequencyinthepopulationhastobe
arecessivetrait.
1947 Youarestudyingadiploidyeaststrainthatnormallyusesglucoseasanenergy
sourcebutcanusemaltosewhennoglucoseispresent.Youareinterestedin
understandinghowthisyeaststrainmetabolizesmaltoseasanalternativeenergy
source.Youisolatethegenesinvolvedinmaltosemetabolismbyscreeningfor
yeastthatcannotgrowwhenmaltoseisthesoleenergysource.Youfindsix
differentmutants,allofwhicharerecessive,andnametheseallelesmal1,mal2,
mal3,mal4,mal5,andmal6.Next,youisolategametesfromthehomozygous
diploidmutantyeaststrainsandperformcrossesbetweenthedifferentstrainsto
docomplementationanalysis,becauseyouwishtodeterminewhetherthe
mutationsarelikelytoaffectthesameordifferentgenes.Yourresultsareshown
inTableQ1947.
TableQ1947Complementationanalysisofmalgenes.
Inhowmanygenesareyoulikelytohaveisolatedmutations?Whichallelesseem
toaffectthesamegenes?Explainyouranswer.
1948 GeneAislocatedneargeneBonchromosome13inhumans.Amutationinthe
germlineofanindividualwiththehaplotypeABgeneratesgameteswiththe
genotypeAb.Manydescendentsofthisfounderindividualcarrythebmutation,
whichpredisposescarrierstohighbloodpressure.Initially,alldescendentswho
inheritthebmutationalsoinherittheneighboringAallele.Throughthe
generations,fewerandfewerdescendentswiththebmutationcarrytheAallele,
andinsteadtheyhavetheaallele.(IndividualswithAandaareequallyhealthy
andfit.)ExplainhowthebandAallelesareseparated.
1949 ShowninFigureQ1949isageneticpedigreeofafamilywithseveralmembers
affectedbyaheritabledisease.Affectedindividualsareshowninblackand
healthyindividualsareshowninwhite.Malesareshownasboxesandfemalesas
circles.Canasinglemutationexplainthepatternofinheritance?Isthemutation
responsibleforthediseasedominantorrecessive?Isthemutationcarriedonthe
Xchromosome,theYchromosome,oranautosome?
FigureQ1949
1950 Thesinglenucleotidepolymorphismsfoundinthehumanpopulation
__________________.
(a)
areimportantforgeneticmappingbecausetheyrepresentmutationsin
genesimportantforhumandisease
(b)
arerarelyfoundamongbloodrelatives
(c)
canbelinkedintohaplotypeblocks
(d)
arosemainlyduringthepast10,000years
How We Know: Using SNPs to Get a Handle on Human Disease

1951 Youaretryingtomapahumangenethoughttobeinvolvedincatallergies.
Becauseyouknow
thisgeneison
chromosome20,
youdecidetoexamine
thelinkageof
severalSNPslocated
onchromosome20
withrespecttothe
geneinvolvedin
catallergies.Youhave
obtainedDNAfrom10individuals,andyouknowwhethertheyareallergicto
cats.YourSNPresultsareshowninTableQ1951.
TableQ1951SNPtestsforchromosome20.(+indicatesthepresenceofSNP.)
A.
B.
WhichSNPismostlikelytobetightlylinkedtothegeneinvolvedincat
allergies?Explainyouranswer.
OftheSNPstestedabove,whichislikelytobethenextclosesttothegene
responsiblefortheallergicstate?Why?
1952 Anytwohumanbeingstypicallyhaveanestimated0.1%differenceintheir
nucleotidesequences,whichisequivalenttoabout3millionnucleotide
differences.ThesedifferencesarethebasisoftheSNPsusedtoconstructgenetic
linkagemaps.SomeoftheseSNPsactuallylieintheregionoftheDNAthat
codesfortheprotein,yettheyhavenoeffectonthephenotypeofindividuals
carryingtheSNPonbothhomologouschromosomes.ExplainhowsomeSNPs
canliewithintheportionoftheDNAthatcodesfortheproteinandyethaveno
discernibleeffectontheproteinsactivity.
1953 FindingcoinheritanceofaSNPvariantandadiseasetellsscientiststhat
____________________.
(a)
everybodywhocarriesthisSNPwillgetthedisease
(b)
sequenceswithintheSNPcausethedisease
(c)
ageneimportantforcausingthediseaseislinkedtotheSNP
(d)
SNPsonotherchromosomeswillnotbecoinheritedwiththedisease
1954 YoudecidetocarryoutgeneticassociationstudiesandidentifyaSNPvariantthat
isfoundsignificantlymoreofteninindividualswhohaveschizophreniathanin
thosewhoarenotaffected.ThisSNPisfoundwithinanintronoftheSZPgene.
A.
CanyoudeducethatanabnormalityoftheSZPgeneisacauseof
increasedriskofschizophrenia?
B.
CanyousaywhethertheSNPvariantitselfisacause?
CHAPTER 20
CELLULAR COMMUNITIES: TISSUES, STEM
CELLS, AND CANCER
Extracellular Matrix and Connective Tissues

201
Bothmulticellularplantsandanimalshave_____________________.
(a)
cellscapableoflocomotion
(b)
cellswithcellwalls
(c)
acytoskeletoncomposedofactinfilaments,microtubules,and
intermediatefilaments
(d)
tissuescomposedofmultipledifferentcelltypes
202
orphraseonlyonce.
Plantsaresedentaryandthustheircellshavedifferentneedsfrom
thoseofcellsfoundinmotileanimals.Forexample,inplantcells,
__________________generatestheturgorpressurethatdrivescell
growth.Plantshavecellwalls,butcellgrowthispossibleinthe
developingtissuebecausethe__________________cellwallsare
expandable.The__________________cellwallsaredeposited
oncegrowthhasstopped,andcanbespeciallyadaptedtotheir
function.Fibersmadefrom__________________(themost
abundantorganicmacromoleculeonEarth)arefoundinplantcell
walls,andprovidetensilestrength.Inwoodytissues,the
__________________inthecellwallsmakesthetissuemorerigid
andwaterproof.Thedepositionofthecellwallisdirectedbythe
__________________cytoskeleton.
cellulose
collagen
epidermis
nuclear
pectin
203
lignin
membranous
osmosis
lamin
primary
secondary
microtubule
tertiary
actin
Whichofthefollowingstatementsaboutplantcellwallsistrue?
(a)
Themicrotubulecytoskeletondirectstheorientationinwhichcelluloseis
depositedinthecellwall.
(b)
(c)
(d)
204
Themolecularcomponentsofthecellwallarethesameinallplant
tissues.
Becauseplantcellwallsarerigid,theyarenotdepositeduntilthecellhas
stoppedgrowing.
Thecellulosefoundincellwallsisproducedasaprecursormoleculein
thecellanddeliveredtotheextracellularspacebyexocytosis.
IndicatethedirectioninwhichtheplantcellshowninFigureQ204ismostlikely
togrow.Theblacklinesindicatethedirectionofthecellulosemicrofibrilsaround
thecell.Explainyouranswer.
FigureQ204
205
Whichofthefollowingmoleculesarenotfoundinplants?
(a)
cellulose
(b)
lignin
(c)
collagen
(d)
pectin
206
Indicatewhetherthefollowingmoleculesarefoundinplants,animals,orboth.
A.
B.
cellwalls
C.
microtubules
D.
cellulose
E.
collagen
207
Whichofthefollowingstatementsaboutanimalconnectivetissuesistrue?
(a)
Enzymesembeddedintheplasmamembranesynthesizethecollagenin
theextracellularmatrixextracellularly.
(b)
Inconnectivetissue,theintermediatefilamentswithinthecellsare
importantforcarryingthemechanicalload.
(c)
Cellscanattachtoacollagenmatrixbyusingfibronectin,anintegral
membraneprotein.
(d)
Proteoglycanscanresistcompressionintheextracellularmatrix.
208
Amajordistinctionbetweentheconnectivetissuesinananimalandothermain
tissuetypessuchasepithelium,nervoustissue,ormuscleis_______________.
(a)
theabilityofconnectivetissuecellssuchasfibroblaststochangeshape
(b)
theamountofextracellularmatrixinconnectivetissues
(c)
theabilityofconnectivetissuestowithstandmechanicalstresses
(d)
209
thenumerousconnectionsthatconnectivetissuecellsmakewitheach
other
Whatarethemainstructuresprovidingtensilestrengthinthefollowing?
A.
animalconnectivetissue
B.
animalepidermis
C.
plantcellwalls
Likemanyotherextracellularproteins,newlysynthesizedcollagen
moleculesundergoposttranslationalprocessinginsidethecellto
convertthemintotheirmatureform;theyarethensecretedand
selfassembleintofibrilsintheextracellularspace.
2011 Fibroblastsorganizethecollagenoftheextracellularmatrixby______________.
(a)
cuttingandrejoiningthefibrils
(b)
processingprocollagenintocollagen
(c)
twistingfibrilstogethertomakeropelikefibers
(d)
pullingthecollagenintosheetsorcablesafterithasbeensecreted
2012 MatchthefourletteredlinesinFigureQ2012withtheappropriatenumbered
label.
FigureQ2012
1.integrin
2.actin
3.collagen
4.fibronectin
2013 Whichofthefollowingstatementsaboutintegrinsisfalse?
(a)
Integrinsuseadaptorproteinstointeractwiththemicrotubule
cytoskeleton.
(b)
Integrinscanswitchtoanactivatedstatebybindingtoanextracellular
matrixmolecule.
(c)
Integrinscanswitchtoanactivatedstatebybindingtoanintracellular
protein.
(d)
Anactivatedintegrinmoleculetakesonanextendedconformation.
2014 Proteoglycansintheextracellularmatrixofanimaltissues________________.
(a)
chieflyprovidetensilestrength
(b)
allowcartilagetoresistcompression
(c)
arelinkedtomicrotubulesthroughtheplasmamembrane
(d)
arepolysaccharidescomposedofglucosesubunits
(a)
Proteoglycanscanactasfilterstoregulatewhichmoleculespassthrough
theextracellularmedium.
(b)
Thenegativechargeassociatedwithproteoglycansattractscations,which
causewatertobesuckedintotheextracellularmatrix.
(c)
Proteoglycansareamajorcomponentofcompactconnectivetissuesbut
arerelativelyunimportantinwaterytissuessuchasthejellylikesubstance
intheinterioroftheeye.
(d)
Glycosaminoglycansarecomponentsofproteoglycan.
Epithelial Sheets and Cell Junctions

orphraseonlyonce.
__________________ join the intermediate filaments in one cell to
those in the neighboring cell. __________________ anchor
intermediate filaments in a cell to the extracellular matrix.
__________________ involve cadherin connections between
neighboring cells and are anchorage sites for actin filaments.
__________________permit the passage of small molecules from
one cell to its adjacent cell. __________________ prevent the
leakage of molecules between adjacent cells.
adherens junctions
desmosomes
gap junctions
hemidesmosomes
highway junctions
tight junctions
2017 LabelthefivedifferenttypesofcellcelljunctionshowninFigureQ2117,and
identifytheapicalandbasalsurfacesoftheepithelium.
Figure Q20-17
2018 Matchthemolecules(list1)withthecellstructuresinwhichtheyareinvolved
(list2).Acellstructuremaybelistedmoreorlessthanonce.
2019 Abasallamina______________________.
(a)
isathinlayerofconnectivetissuecellsandmatrixunderlyingan
epithelium
(b)
isathinlayerofextracellularmatrixunderlyinganepithelium
(c)
isattachedtotheapicalsurfaceofanepithelium
(d)
separatesepithelialcellsfromeachother
2020 Tightjunctions______________________.
(a)
allowsmallwatersolublemoleculestopassfromcelltocell
(b)
interactwiththeintermediatefilamentsinsidethecell
(c)
(d)
areformedfromclaudinsandoccludins
arefoundincellsinconnectivetissues
2021 Adherensjunctions______________________.
(a)
canbeusedtobendepithelialsheetsintotubes
(b)
aremostoftenfoundatthebasalsurfaceofcells
(c)
arefoundonlyinadulttissues
(d)
involvefibronectinandintegrininteractions
2022 Atdesmosomes,cadherinmoleculesareconnectedto________________.
(a)
actinfilaments
(b)
(c)
microtubules
(d)
gapjunctions
2023 Hemidesmosomesareimportantfor______________________.
(a)
tubulationofepithelialsheets
(b)
linkagestoglycosaminoglycans
(c)
formingthebasallamina
(d)
attachingepithelialcellstotheextracellularmatrix
2024 Whichofthefollowingstatementsaboutgapjunctionsisfalse?
(a)
Gapjunctionsaremadeofconnexons.
(b)
Moleculesupto1000daltonsinmolecularweightcanmoveacrossgap
junctions.
(c)
Becausegapjunctionsdonotallowionstopassthrough,theyarenotused
forelectricallycouplingcells.
(d)
Gapjunctionscancloseinresponsetoextracellularsignals.
2025 Whichtypeofjunctioninvolvesaconnectiontotheactincytoskeleton?
(a)
adherensjunctions
(b)
desmosomes
(c)
tightjunctions
(d)
gapjunctions
2026 Whichtypeofjunctioncontributesthemosttothepolarizationofepithelialcells?
(a)
adherensjunctions
(b)
desmosomes
(c)
tightjunctions
(d)
gapjunctions
2027 Cadherins______________________.
(a)
areusedtotransferproteinsfromonecelltoanother
(b)
mediatecellcellattachmentsthroughhomophilicinteractions
(c)
(d)
areabundantintheplantcellwall
bindtocollagenfibrils
2028 Plasmodesmata______________________.
(a)
permitsmallmoleculestopassfromonecelltoanother
(b)
arefoundonlyinanimalcells
(c)
areclosedbytheneurotransmitterdopamine
(d)
providetensilestrength
Tissue Maintenance and Renewal

2029 Matchtheappropriatecelltypefoundinthemammalianskinwiththebest
descriptionofitsfunction.
2030 Namethethreekeymechanismsimportantformaintainingtheorganizationof
cellsintotissues.
2031 Placethefollowinginorderoftheirreplacementtimes,fromshortesttolongest.
A.
epidermal cell
B.
nerve cell
C.
bone matrix
D.
red blood cell
E.
cell lining the gut
2032 Cellsthatareterminallydifferentiated______________________.
(a)
willundergoapoptosiswithinafewdays
(b)
cannolongerundergocelldivision
(c)
areunabletomove
(d)
nolongerproduceRNAs
2033 Anadulthemopoieticstemcellfoundinthebonemarrow
______________________.
(a)
willoccasionallyproduceepidermalcellswhennecessary
(b)
canproduceonlyredbloodcells
(c)
canundergoselfrenewingdivisionsforthelifetimeofahealthyanimal
(d)
willexpressallthesametranscriptionfactorsasthosefoundinan
unfertilizedegg
2034 Mouseembryonicstem(ES)cells______________________.
(a)
canonlybeproducedthroughtherapeuticcloning
(b)
cangiverisetoalltissuesandcelltypesinthebodyexceptgermcells
(c)
canbeimplantedinfostermotherstoproduceclonedcowsandother
animals
(d)
comefromtheinnercellmassofearlyembryos
2035 Howdoreproductivecloningandtherapeuticcloningdiffer?
(a)
TheDNAinthenucleusofcellsproducedfortherapeuticcloningis
geneticallyidenticaltothedonorgenome,whereasincellsproducedfor
reproductivecloningitisnot.
(b)
Reproductivecloningrequiresasupplyoffertilizeddonoreggcells,
whereastherapeuticcloningrequiresunfertilizedeggcells.
(c)
Therapeuticcloningrequiresnucleartransplantation,whereasreproductive
cloningdoesnot.
(d)
Embryosareplacedintofostermothersduringreproductivecloningbut
notduringtherapeuticcloning.
2036 Inducedpluripotentstem(iPS)cells______________________.
(a)
arecreatedbytheexpressionofasetofkeygenesincellsderivedfrom
adulttissuessothatthesecellscandifferentiateintoavarietyofcelltypes
(b)
requireasupplyofdonoreggcells,suchasembryonicstemcells
(c)
candifferentiateintoagreatervarietyofadulttissuesthanembryonicstem
cells
(d)
arecreatedbynucleartransplantation
2037 Astemcelldividesintotwodaughtercells.Oneofthedaughtercellsgoesonto
becomeaterminallydifferentiatedcell.Whatisthetypicalfateoftheother
daughter cell?
2038 YourfriendisapioneerinEScellresearch.Inherresearch,sheusesanEScell
linethatoriginatedfromaninbredstrainoflaboratorymicecalledFG426.She
hasjustfiguredoutmethodsthatallowhertogrowanentireliverfromanEScell
andhassuccessfullygrown10livers.Shedemonstratesthatthenewlygrown
liversarefunctionalbysuccessfullytransplantingoneofthenewliversintoa
FG426laboratorymouse.
Youareparticularlyexcitedaboutthis,becauseyouhaveasickpetmouse,
Squeaky.YouareveryattachedtoSqueaky,asyoufoundhimwhenyouwereout
campinginNewHampshire.Unfortunately,Squeakyhasdevelopedliverdisease
andwillnotlivemuchlongerwithoutalivertransplant.Afteryouseeyourfriend
onTVtalkingabouthernewmethodforgrowingmouselivers,youimmediately
grabyourcellphonetoaskherwhetherSqueakycouldhaveoneofthenewly
grownlivers.Justasyouareabouttodialyourfriend,youremembersomething
youlearnedincellbiologyandrealizethatinstead,youshouldaskyourfriend
aboutpossiblyusingtherapeuticcloningforSqueakysbenefit.
A.
Whydoyouthinkthatoneofthenewlygrownliversmaynotworkin
Squeaky?
B.
Explainwhytherapeuticcloningwouldsolvethisproblem.
Cancer
2039 Amalignanttumorismoredangerousthanabenigntumorbecause
______________________.
(a)
itscellsareproliferatingfaster
(b)
itcausesneighboringcellstomutate
(c)
itscellsattackandphagocytoseneighboringnormaltissuecells
(d)
itscellsinvadeothertissues
2040 Whichofthefollowingstatementsaboutcancerisfalse?
(a)
Virusescausesomecancers.
(b)
Tobaccouseisresponsibleformorethan20%ofallcancerdeaths.
(c)
Amutationinevenasinglecancercriticalgeneissufficienttoconverta
normalcellintoacancercell.
(d)
Chemicalcarcinogenscausecancerbychangingthenucleotidesequence
ofDNA.
2041 Cancerisadiseaseofenhancedproliferationandcellsurvival.DNArepair
mechanisms are normally important for cell survival. When a cell senses DNA
damage, the cell cycle is inhibited until the damage is fixed. Given the importance
of DNA repair mechanisms, how can their failure can lead to the production of
cancer cells with a competitive advantage over normal cells?
2042 Whichofthefollowinggeneticchangescannotconvertaprotooncogeneintoan
oncogene?
(a)
Amutationthatintroducesastopcodonimmediatelyafterthecodonfor
theinitiatormethionine.
(b)
Amutationwithinthecodingsequencethatmakestheproteinhyperactive.
(c)
Anamplificationofthenumberofcopiesoftheprotooncogene,causing
overproductionofthenormalprotein.
(d)
Amutationinthepromoteroftheprotooncogene,causingthenormal
proteintobetranscribedandtranslatedatanabnormallyhighlevel.
2043 Whichofthefollowingstatementsabouttumorsuppressorgenesisfalse?
(a)
Geneamplificationofatumorsuppressorgeneislessdangerousthangene
amplificationofaprotooncogene.
(b)
Cellswithonefunctionalcopyofatumorsuppressorgenewillusually
proliferatefasterthannormalcells.
(c)
(d)
Inactivationoftumorsuppressorgenesleadstoenhancedcellsurvivaland
proliferation.
Individualswithonlyonefunctionalcopyofatumorsuppressorgeneare
morepronetocancerthanindividualswithtwofunctionalcopiesofa
tumorsuppressorgene.
2044 Acertainmutationinthereceptorforepidermalgrowthfactor(EGF)causesthe
mutatedreceptorproteintosendapositivesignalalongtheassociated
intracellularsignalingpathwayevenwhentheEGFligandisnotboundtoit.This
signalleadstoabnormalcellproliferationintheabsenceofgrowthfactor.Onthe
basisofthisinformation,wouldyouclassthegenefortheEGFreceptorasa
tumorsuppressorgeneorapotentialoncogene?Explainyouranswer.
2045 RasisaGTPbindingproteinthatisoftendefectiveincancercells.Asignalfrom
agrowthfactorthroughareceptortyrosinekinaseoftenstimulatesnormalcellsto
divide.Whenthereceptortyrosinekinasebindsthegrowthfactor,Rasis
stimulatedtobindGTP.Rasinturnactivatesproteinsthatpromotecell
proliferation.AcommonmutationincancerouscellscausesRastobehaveas
thoughitwereboundtoGTPallthetime.
A.
Whyisthismutationadvantageoustocancerouscells?
B.
YourfrienddecidesthatthesignalingpathwayinvolvingtheRasprotein
isagoodtargetfordrugdesign,becausetheRasproteinisoftendefective
incancercells.Yourfrienddesignsadrugthatwillturnoffthereceptor
tyrosinekinasebypreventingitfromdimerizing.Doyouthinkthatthis
drugwillaffectcellsthathaveadefectiveRasproteinthatactsasifit
werealwaysboundtoGTP?Whyorwhynot?
2046 PeoplewhoinheritonecopyoftheRb(retinoblastoma)genethatisnormaland
onecopythatismutatedthatis,peoplewhoareheterozygousforRbhavea
greatlyincreasedriskofcancer.
Given this information, do you agree or disagree with the following statement?
Explain your answer.
TheRbmutationmusthaveadominanteffect,whichmeansthatit
mustresultinanincreaseinRbfunction.Thus,Rbinitsmutant
formmustbe
anoncogene.
2047 FigureQ2047
mutationsthatmight
developmentof
Explainwhytheloss
advantageousto
showsasequenceof
underliethe
colorectalcancer.
ofp53is
cancerouscells.
Figure Q20-47
2048 Drugsthatblockthefunctionofoncogenicproteinsholdgreatpromiseinthe
fightagainstcancer.Shouldcancerresearchersalsobeattemptingtodesigndrugs
thatwillinterferewiththeproductsoftumorsuppressorgenes?Explain.
2049 Rbisatumorsuppressorgene;itsnormalfunctionistohelprestraincelldivision.
LossofbothcopiesofRbisacausativefactorinsomekindsofcancer.You
proposetotreatthesecancersbyinjectingthepatientswithaviralvectorthat
carriesacopyoftheRbgeneandhastheabilitytoinfectallthecellsofthebody,
therebyartificiallydrivingexpressionofRbinallthecells,includingthecancer
cells.YourcolleaguesaysNo!You'llsimplykillthepatient,becauseyouwill
haltcelldivisionthroughoutthebody.
A.
Whywouldhaltingcelldivisionthroughoutthebodykillafullgrown
adultperson?
B.
IsyourcolleaguerightinthinkingthatforcedexpressionofRbinevery
cellwillhaltallcelldivision?
2050 In1971,DrJudahFolkmanpublishedtheangiogenichypothesissuggestingthat
atumorcannotgrowbeyond12millimeterswithoutthedevelopment
(angiogenesis)ofnewbloodvesselsthatprovideaccesstooxygenandnutrients.
Duringthe1990s,itwasdiscoveredthatvascularendothelialgrowthfactor
(VEGF)stimulatestheproliferationandmigrationofthecellsthatformblood
vessels,leadingtotheformationofnewbloodvessels.VEGFbindstoreceptor
tyrosinekinases(RTKs)onthecellsurfaceandcausestheRTKstodimerizeand
becomeactive,therebyinitiatinganintracellularsignalingcascadethatstimulates
celldivisionandinhibitsapoptosis.Manycancercellssecretehighlevelsof
VEGF.IncreasedVEGFexpressioninatumoriscorrelatedwithapoormedical
outcomeforthepatient.SomeevidencesuggeststhatblockingVEGFdependent
signalingmaypreventtheformationofnewbloodvesselsandleadtothedeathof
immaturebloodvesselswithoutdisturbingmaturebloodvessels.Youworkfora
biotechnologycompanythatseekstocreateanticancerdrugsthatpreventthe
growthoftumorsand/orcausetumorstoshrink,whileleavingnormalcells
relativelyuntouched.AfterlearningaboutVEGF,youhaveabrightideafora
newmechanismofactionforapotentialanticancerdrug.Whatisyouridea?
How We Know: Making Sense of the Genes that Are Critical for
Cancer
2051 YourstudiesincellbiologyhaverevealedhowAPC,aproteinencodedbya
tumorsuppressorgenethatisfrequentlyinactivatedinpeoplewithcolorectal
cancer,functionsintheWntsignalingpathway(seeFigureQ2051).Thishas
inspiredyoutostudyWntsignaling.Youwouldliketodesignadrugtotreat
peoplewithcolorectalcancer.GiventhepathwayshowninFigureQ2051and
theknowledgethatmosthumancolorectaltumorsharbormutationsintheAPC
gene,nameaproteinfromthepathwaythatwouldbeagoodtargetforanactivity
blockinganticancerdrug.Explainyouranswer.
Figure Q20-51

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What organelle is described that is found in a fungus but not other eukaryotic cells?

What organelle is described that is found in a fungus but not other eukaryotic cells?

What protein in the Wnt signaling pathway would be a good target for an anticancer drug according to the information provided?

What protein in the Wnt signaling pathway would be a good target for an anticancer drug according to the information provided?

CHAPTER 15

INTRACELLULAR COMPARTMENTS AND TRANSPORT

2009 Garland Science Publishing

Which of the following statements about membrane-enclosed organelles is true?

Name the membrane-enclosed compartments in a eucaryotic cell where each of the

amino acid sequence

Where are proteins in the chloroplast synthesized?

15-10 Which of the following statements is true?

The N-terminus of this protein is cytoplasmic.

deleting the first signal sequence

15-37 A plasma membrane

central Golgi cisternae

15-38 Which of the following statements about secretion is true?

Proteins destined for constitutive exocytosis aggregate as a result of the acidic pH

__________________ (sheetlike projections of their plasma membrane) to

a defect in one of the lysosomal hydrolases

How We Know: Tracking Protein and Vesicle Transport

2009 Garland Science Publishing

General Principles of Cell Signaling

chemical signal. Cells receive signals through a

Which of the following statements is false?

All members of the steroid hormone receptor family __________________.

do not undergo conformational changes

QGF activates different intracellular signaling pathways in heart muscles,

16-17 Name the three main classes of cell-surface receptor.

16-23 Indicate by writing yes or no whether amplification of a signal could occur at

addition of a high concentration of a non-hydrolyzable analog of GTP

modification of the G subunit by cholera toxin

Table Q16-27 Mating phenotypes of various strains of yeast

a mutation in the Nerd gene that produces a protein that cannot be

16-29 Adrenaline stimulates glycogen breakdown in skeletal muscle cells by ultimately

the expression of a constitutively active phospholipase C

16-31 A calmodulin-regulated kinase (CaM-kinase) is involved in spatial learning and

A. cleavage of inositol phospholipids

__________________, which also binds diacylglycerol, and

16-41 Which of the following mechanisms is not directly involved in inactivating an

Cells signal to one another in various ways. Some use extracellular

16-45 Which of the following statements is true?

response to PDGF binding, become phosphorylated on whichever tyrosines

From these data, which, if any, of proteins A, B, C, and D are involved in

16-48 Akt promotes the survival of many cells. It is activated by an intracellular

How We Know: Untangling Cell Signaling Pathways

addition of a drug that prevents protein X from activating Ras

Table Q16-54 Chemotaxis in wild-type and mutant strains of bacteria

How We Know: Pursuing Motor Proteins

2009 Garland Science Publishing

Overview of the Cell Cycle

How We Know: Discovery of Cyclins and Cdks

The Cell-Cycle Control System

Control of Cell Number and Cell Size

SEX AND GENETICS

The Benefits of Sex

Meiosis and Fertilization

Mendel and the Laws of Inheritance