C.elegans: A Model To Study Animal Development: 2. History 3. Anatomy 4. Reproduction and Development

C.
elegans : A model to study animal development
CONTENTS
1. Introduction
2. History
3. Anatomy
4. Reproduction and development
1
5. RNA mediate interference

6. Axis formation
7. Development of vulva
8. Apoptosis
9. Conclusion
10. References
I. INTRODUCTION
Caenorhabditis elegans(Gr.caenor-recent, rhabditis-rod like) and (L.elegans-elegant) is a
free living, transparent nematode, 1 mm in length, that lives in soil environment. In 1900,
Maupas initially named Rhabdites elegans, and then Osche changed the name Rhabdites into
Caenorhabditis in 1952. C.elegans is an unsegmented pseudocoelomate, and lack of respiratory
and circulatory system. Majority of these nematodes are hermaphrodites. C.elegans
was the first multicellular organism to have its whole genome sequenced.
II. SYSTEMATIC POSITION
Kingdom - Animalia
Phylum
- Nemathelminthes
Class
- Chromadorea
Order
- Rhabditida
2
Family
- Rhabditidae
Genus
- Caenorhabditis
Species
- elegans
III. HISTORY
In 1963, Sydney Brenner proposed research in C.elegans primarily in the area of
neuronal development. In 1974, he started research in the molecular and developmental biology
of C.elegans, which was since used as a model organism. In 2002, the Nobel Prize in Physiology
or Medicine was awarded to Sydner Brenner, H. Robert Hortivz and John Sulston for their work
on the genetics of organ development and Programmed cell death in C. elegans. 4. In 2006,
Nobel Prize in Physiology or Medicine was awarded to Andrew Fire and Craig C . Mello for
their discovery of RNA interference in C.elegans. In 2008, Martin Chalfie, Roger Y. Tsien and
Osamu Shimomura shared a Nobel Prize in Chemistry for their work on green fluorescent
protein, some of the research involved the use of C. elegans.
IV. C.elegans AS MODEL ORGANISM

The soil nematode C.elegans was choosen as model organism because of following
reasons. It has fewer numbers of cells. It has a small genome. It can easily breed and maintained.
It has short life span. It can be genetically manipulated.
IV.1. ANATOMY OF C.elegans

C.elegans is unsegmented, vermiform, and bilaterally symmetical nematode. It has
cuticle, four main epidermal cords, and a fluid filled pseudocoelom. About one in thousand
individuals are male and rest are hermaphrodites. The basic anatomy of C.elegans includes a
mouth, pharynx, intestine, gonad, and collagenous cuticle.
The pharynx is a muscular food pump in the head of C.elegans which is triangular in cross
section. It grinds food and transports it directly to the intestine. After digestion, the contents of
the intestine are released via the rectum. Males have a single lobed gonad and a tail specialized
for mating, which incorporates spicules. Hermaphrodites have two ovaries, oviducts,
spermatheca, and a single uterus.
Fig. 1 Anatomy of C. elegans
IV.2. REPRODUCTION AND DEVELOPMENT

3
C.elegans has a very rapid life cycle. After fertilization the embryonic development
begins in the hermaphrodites uterus with secretion of a tough chitinous shell around the
fertilized eggs. The large cells, produced by early embryonic cleavage are known as blastomeres.
At 28 cell stage, cell movements start which give rise to basic body plan of larval and adult
stages. After 14 hours of fertilization, the first stage juvenile known as L1 larva, hatches from
the egg cell. Over the next 50 hours, development proceeds through three additional larval stages
L2, L3, and L4 separated from each other by molts. During each molt it synthesizes a new
cuticle under the old and then it sheds the old. 8. The life span of an adult is about 15
days. They grow well at a range of temperature about 25 degree Celsius. The adult
hermaphrodites have 959 somatic cells and males have 1090 somatic cells.
IV.3. NUCLEAR GENOME

The sequencing of genome was completed in 1998. After that C.elegans genome
sequencing consortium
was done in 1999. The result established that the genome size is
about 100 million nucleotide pairs and there are about 18,000-20,000 gene. C.elegans genome is
packaged into six chromosomes i.e. I, II, III, IV, V and X.
Fig. 2 Apoptosis in C.elegans.
IV.4. GENE EXPRESSION

The major mechanism of gene
expression is the trans-splicing of RNAs.
In this process, exons from two separate
RNA transcripts are spliced together to
form a mature RNA molecule. The first
one is the spliced leader sequenced RNA
which is a completely evolutionary
conserved sequence in nematodes. The
spliced leader RNA always has a donor
site. The second one is the pre m-RNA
which does not have a spliced leader
sequence. The splicing is catalyzed by a
spliceosome formed from the assembly of snRNPs and other components.
IV.5. CLONING OF C. elegans GENE

The cloning of C.elegans gene is mainly achieved by positional cloning, based only on
the genes position in the genome. The central core of positional cloning is to find out the genes
responsible for desired phenotypes. The genes responsible for desired phenotypes are called as
candidate genes can be detected by the use of DNA markers. The positioning of a new mutation
between two DNA markers precisely defines the physical interval in which the new gene must
lie. If the candidate is found to be in a sequence homolog to normal, it is the normal phenotype
or homolog with mutant, it is clear that the candidate is in fact the gene responsible.
4
IV.6. RNA MEDIATE INTERFERENCE

In 1998, Fire and Mello first established this in C. elegans. This is the method for
analyzing gene function. Researchers discovered that injection of dsRNA into an adult
hermaphrodite caused the silencing of a specific gene in the injected worm and its progeny. This
phenomenon is known as RNA mediated interference (RNAi). These injected dsRNAs are
processed into small interfering RNAs (siRNAs) by an RNAase III like enzyme, dicer. Dicer
loads the siRNAs into RNA induced silencing complex (RISC). In RISC, the siRNAs break a
passenger strand which becomes degrade during RISC activation and a guide strand which
directs gene silencing. RNAi is an evolutionary conserved mechanism. It has role in post
transcriptional gene regulation, transposon regulation and defending cell against viruses. It is
also known as post transcriptional gene silencing.
IV.7. AXIS SPECIFICATION

The specifications of axis are the product of maternal effect gene, which the mother
supplied to the egg during oogenesis. The decision as to which end will become anterior and
which the posterior, seems to reside with the position of the sperm nucleus. The entrance end of
sperm pronucleus is the anterior and the opposite becomes the posterior pole. Originally PAR -3
and MEX -5 proteins are seen to be throughout the egg, the former in the cortex and later spread
throughout the egg cytoplasm. Near the newly formed sperm aster, PAR-2 replaces PAR -3 in the
cortical cytoplasm. After the first cell division, the AB blastomers has PAR-3 and MEX-5, while P
cell contains cortical PAR -2. The most important entities localized in PAR proteins are Pgranules. Shortly after fertilization the P-granules migrates to posterior pole and enter in to P-cell
lineage. The former AB blastomere indicates the anterior
pole. The ABp cell defines the dorsal
and EMS cell defines the ventral while MS cell contracts with ABa cell distinguish the right side
from the left.
IV.8. DEVELOPMENT OF VULVA

Vulva is the passage way through which sperm from the male enter and fertilized eggs
exit the gonad. In vulva development first six vulval precursor cells (VPCs) are born. These are
hypodermal in origin. All VPCs are present on the ventral side of the gonads. These cells are
numbered as P3, P4, P5, P6, P7 and P8. The anchor cell of the gonad secretes LIN-3, acts on
central VPC (P6) which forms central vulval cells. The P5 and P7 VPCs receive the signal
through LET - 23 receptor on the cell membrane, involved in forming lateral vulval cells. The
lateral VPCs do not instruct the peripheral VPCs to do anything, so they become hypodermis.
IV.9. APOPTOSIS
Cell death is as important as cell proliferation in development. During apoptosis the
affected cell shrinks, degrade its DNA and die, after which they are engulfed and digested by
neighboring cell. The function of apoptosis seems to be elimination of unneeded cells that could
be detrimental to the organism. The genes that are responsible for apoptosis are cell for death
(CED) genes. CED-3 is a member of caspase family of proteases, are essential for apoptosis.CED4 protein is required for the activation of CED-3.CED-9 is anti -apoptotic in nature. In C. elegans
this process helps in controlling the size of the cell population by eliminating excess unwanted
cells.
5
Fig. 3 Apoptosis in C.elegans.
V. CONCLUSION
Studies of C.elegans can help to elucidate developmental pathways and genes conserved
throughout animal evolution. Despite some unusual features, C.elegans shares most of its
regulatory pathways with other multicellular animals.
VI. REFERENCE
1. Ellis H M and Horvitz H R (1986) Genetic control of programmed cell death in the
nematode C.elegans . Cell, 44 (6) pp 817-819.
2. Gilbert S F (2006) Developmental Biology. 8th Edition, Sinauer Associates Inc.
Publishers Massachusetts, USA, pp 1-117.
3. Slack W M J (2006) Essential Developmental Biology. 2nd Edition, Blackwell Publishing,
USA, pp 1-365.

C.elegans: A Model To Study Animal Development: 2. History 3. Anatomy 4. Reproduction and Development

Uploaded by

Copyright:

Available Formats

C.elegans: A Model To Study Animal Development: 2. History 3. Anatomy 4. Reproduction and Development

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

C.elegans: A Model To Study Animal Development: 2. History 3. Anatomy 4. Reproduction and Development

Uploaded by

Copyright:

Available Formats

C.

elegans : A model to study animal development

5. RNA mediate interference

IV. C.elegans AS MODEL ORGANISM

IV.1. ANATOMY OF C.elegans

Fig. 1 Anatomy of C. elegans

IV.2. REPRODUCTION AND DEVELOPMENT

IV.3. NUCLEAR GENOME

IV.4. GENE EXPRESSION

IV.5. CLONING OF C. elegans GENE

IV.6. RNA MEDIATE INTERFERENCE

IV.7. AXIS SPECIFICATION

IV.8. DEVELOPMENT OF VULVA

Fig. 3 Apoptosis in C.elegans.

You might also like