Papers by Michael Barresi
Elsevier eBooks, 2020
Abstract Whether human, bird, or fish, all organisms with a backbone look quite similar at one co... more Abstract Whether human, bird, or fish, all organisms with a backbone look quite similar at one common point in their lives—during the earliest life stage, the time of embryogenesis. The complex form of an adult organism originated from the diversification of much simpler beginnings as an embryo. From the fusion of two haploid genomes, a single-celled zygote is conceived. This earliest staged embryo is tasked with the challenge of building many more cells while simultaneously establishing the basic positional locations of the head, tail, back, and belly. The zebrafish model system was itself conceived for the main purpose of investigating the genetics governing vertebrate embryogenesis (See also Chapter 1; Anderson & Ingham, 2003; Grunwald & Eisen, 2002; Li, Huang, Dong, Zhu, & Liu, 2013; Meunier, 2012). In this chapter, we will discuss the many advantages and novel insights the zebrafish model system has brought to our understanding of the developmental biology governing vertebrate embryogenesis.
American Journal of Medical Genetics, Mar 20, 2017
Evolution & Development, 2006
The somitic compartment that gives rise to trunk muscle and dermis in amniotes is an epithelial s... more The somitic compartment that gives rise to trunk muscle and dermis in amniotes is an epithelial sheet on the external surface of the somite, and is known as the dermomyotome. However, despite its central role in the development of the trunk and limbs, the evolutionary history of the dermomyotome and its role in non-amniotes is poorly understood. We have tested whether a tissue with the morphological and molecular characteristics of a dermomyotome exists in non-amniotes. We show that representatives of the agnathans and of all major clades of gnathostomes each have a layer of cells on the surface of the somite, external to the embryonic myotome. These external cells do not show any signs of terminal myogenic or dermogenic differentiation. Moreover, in the embryos of bony fishes as diverse as sturgeons (Chondrostei) and zebrafish (Teleostei) this layer of cells expresses the pax 3 and 7 genes that mark myogenic precursors. Some of the pax7expressing cells also express the differentiation-promoting myogenic regulatory factor Myogenin and appear to enter into the myotome. We therefore suggest that the dermomyotome is an ancient and conserved structure that evolved prior to the last common ancestor of all vertebrates. The identification of a dermomyotome in fish makes it possible to apply the powerful cellular and genetic approaches available in zebrafish to the understanding of this key developmental structure.
Development, May 15, 2000
Hedgehog proteins mediate many of the inductive interactions that determine cell fate during embr... more Hedgehog proteins mediate many of the inductive interactions that determine cell fate during embryonic development. Hedgehog signaling has been shown to regulate slow muscle fiber type development. We report here that mutations in the zebrafish slow-muscle-omitted (smu) gene disrupt many developmental processes involving Hedgehog signaling. smu −/− embryos have a 99% reduction in the number of slow muscle fibers and a complete loss of Engrailed-expressing muscle pioneers. In addition, mutant embryos have partial cyclopia, and defects in jaw cartilage, circulation and fin growth. The smu −/− phenotype is phenocopied by treatment of wildtype embryos with forskolin, which inhibits the response of cells to Hedgehog signaling by indirect activation of cAMP-dependent protein kinase (PKA). Overexpression of Sonic hedgehog (Shh) or dominant negative PKA (dnPKA) in wild-type embryos causes all somitic cells to develop into slow muscle fibers. Overexpression of Shh does not rescue slow muscle fiber development in smu −/− embryos, whereas overexpression of dnPKA does. Cell transplantation experiments confirm that smu function is required cell-autonomously within the muscle precursors: wild-type muscle cells rescue slow muscle fiber development in smu −/− embryos, whereas mutant muscle cells cannot develop into slow muscle fibers in wild-type embryos. Slow muscle fiber development in smu mutant embryos is also rescued by expression of rat Smoothened. Therefore, Hedgehog signaling through Slow-muscle-omitted is necessary for slow muscle fiber type development. We propose that smu encodes a vital component in the Hedgehog response pathway.
Developmental Neurobiology, Apr 3, 2021
for all their supportive contributions during the course of this research. We would also like to ... more for all their supportive contributions during the course of this research. We would also like to thank the Smith College Center for Microscopy and its manager, Judith Wopereis, and the Smith Animal Care facility for their constant support and technical assistance throughout this work. Lastly, we are extremely appreciative of all constructive discourse provided by the entire Barresi lab from the first experiments to the final manuscript.
Developmental Biology, Mar 1, 2014
Radial glia serve as the resident neural stem cells in the embryonic vertebrate nervous system, a... more Radial glia serve as the resident neural stem cells in the embryonic vertebrate nervous system, and their proliferation must be tightly regulated to generate the correct number of neuronal and glial cell progeny in the neural tube. During a forward genetic screen, we recently identified a zebrafish mutant in the kif11 loci that displayed a significant increase in radial glial cell bodies at the ventricular zone of the spinal cord. Kif11, also known as Eg5, is a kinesin-related, plus-end directed motor protein responsible for stabilizing and separating the bipolar mitotic spindle. We show here that Gfap þ radial glial cells express kif11 in the ventricular zone and floor plate. Loss of Kif11 by mutation or pharmacological inhibition with S-trityl-L-cysteine (STLC) results in monoastral spindle formation in radial glial cells, which is characteristic of mitotic arrest. We show that M-phase radial glia accumulate over time at the ventricular zone in kif11 mutants and STLC treated embryos. Mathematical modeling of the radial glial accumulation in kif11 mutants not only confirmed an $ 226 Â delay in mitotic exit (likely a mitotic arrest), but also predicted two modes of increased cell death. These modeling predictions were supported by an increase in the apoptosis marker, anti-activated Caspase-3, which was also found to be inversely proportional to a decrease in cell proliferation. In addition, treatment with STLC at different stages of neural development uncovered two critical periods that most significantly require Kif11 function for stem cell progression through mitosis. We also show that loss of Kif11 function causes specific reductions in oligodendroglia and secondary interneurons and motorneurons, suggesting these later born populations require proper radial glia division. Despite these alterations to cell cycle dynamics, survival, and neurogenesis, we document unchanged cell densities within the neural tube in kif11 mutants, suggesting that a mechanism of compensatory regulation may exist to maintain overall proportions in the neural tube. We propose a model in which Kif11 normally functions during mitotic spindle formation to facilitate the progression of radial glia through mitosis, which leads to the maturation of progeny into specific secondary neuronal and glial lineages in the developing neural tube.
3D rendering of confocal z-stack of a 48 hpf tg(fli1a:gfp) (green) embryo labeled with anti-AT (b... more 3D rendering of confocal z-stack of a 48 hpf tg(fli1a:gfp) (green) embryo labeled with anti-AT (blue). Left panel rotates clockwise around the anterior-posterior vertical axis, starting from a ventral perspective. The right panel shows the same sample rotating clockwise around the anterior-posterior horizontal axis, starting from a lateral perspective and moving towards a dorsal perspective
3D rendering of a 36 hpf tg(fli1a:gfp) (green) forebrain immunolabeled with anti-AT (blue). Left ... more 3D rendering of a 36 hpf tg(fli1a:gfp) (green) forebrain immunolabeled with anti-AT (blue). Left panel begins from a frontal perspective and rotates clockwise 300◦ around the anterior-posterior axis. The right panel is the same sample and begins from a more dorsal perspective and rotates in phase with the left panel
Scrolling through frontal z-stack of a 22 hpf tg(gfap:nls-mcherry (magenta); olig2:gfp (green) em... more Scrolling through frontal z-stack of a 22 hpf tg(gfap:nls-mcherry (magenta); olig2:gfp (green) embryo labeled for pH3 (blue). Movie begins at the most superficial/anterior slice and scrolls to deeper/more posterior slices, spanning the entire commissural region
Scrolling through frontal z-stack of a 24 hpf tg(gfap:nls-mcherry (magenta); olig2:gfp (green)) f... more Scrolling through frontal z-stack of a 24 hpf tg(gfap:nls-mcherry (magenta); olig2:gfp (green)) forebrain labeled with anti-HuC/D (blue). Movie begins at the most superficial/anterior slice and scrolls to deeper/more posterior slices, spanning the entire commissural region
3D rendering of tg(olig2:gfp) (green) forebrain immunolabeled with anti-AT (blue). Left panel beg... more 3D rendering of tg(olig2:gfp) (green) forebrain immunolabeled with anti-AT (blue). Left panel begins from a frontal perspective and rotates clockwise 360◦ around the anterior-posterior axis. The right panel is the same sample and begins from a more dorsal perspective and rotates in phase with the left panel. AT signal intensity is increased for structural visualization purposes
3D rendering of confocal z-stack of a 48 hpf tg(olig2:gfp) (green) embryo labeled with anti-AT (b... more 3D rendering of confocal z-stack of a 48 hpf tg(olig2:gfp) (green) embryo labeled with anti-AT (blue). Left panel rotates clockwise around the anterior- posterior vertical axis, starting from a ventral perspective. The right panel shows the same sample rotating counterclockwise around the anterior-posterior horizontal axis, starting from a lateral perspective and moving towards a dorsal perspective
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Papers by Michael Barresi