Characterization of transcription factor PAX-3 in the gene regulatory network that specifies hypodermal cell fate in C. elegans
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Date
2020-01-20
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Department
Biological Sciences
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Biological Sciences
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Distribution Rights granted to UMBC by the author.
This item may be protected under Title 17 of the U.S. Copyright Law. It is made available by UMBC for non-commercial research and education. For permission to publish or reproduce, please see http://aok.lib.umbc.edu/specoll/repro.php or contact Special Collections at speccoll(at)umbc.edu
This item may be protected under Title 17 of the U.S. Copyright Law. It is made available by UMBC for non-commercial research and education. For permission to publish or reproduce, please see http://aok.lib.umbc.edu/specoll/repro.php or contact Special Collections at speccoll(at)umbc.edu
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Abstract
The process of organogenesis requires the coordination of a series of cellular events that need to be tightly regulated for proper development. One of the early steps in organogenesis is cell-fate specification, and the question of how cells are specified to adopt different fates from each other is a central one in developmental biology. The formation of the C. elegans skin (the hypodermis) is an excellent model to study how general categories of cell types, such as hypodermal cells, acquire a specific cell fate. Early events in C. elegans embryogenesis induce hypodermal precursor cells to follow one of several paths of differentiation, among them, becoming dorsal, lateral or ventral hypodermal cells. The regulatory network that drives this hypodermal cell fate specification is an intriguing process for which much remains to be understood: since the small number of genetic interactions described so far indicates that there may be a number of additional unknown regulators involved in hypodermal cell fate specification. The Eisenmann lab has previously studied the role of signaling pathways and transcription factors in the specification of hypodermal cell fates during larval life, focusing on the development of the ventral and lateral hypodermal cells. However, much less is known about the differential gene expression programs that make these hypodermal cells adopt different fates during embryonic development. Work done previously in the Eisenmann lab showed that the conserved paired-box transcription factor PAX-3 is expressed in the embryonic ventral hypodermis and is required to prevent the ventral hypodermal cells from adopting a lateral hypodermal (seam cell) fate (Thompson et al., 2016). The importance of pax-3 in the specification of the hypodermis in C. elegans is evident from the severity of the hypodermal phenotypes observed in pax-3 mutants: complete loss of pax-3 leads to embryonic lethality. My research seeks to further understand the role of pax-3 in specifying the ventral hypodermal cells early during embryonic development in C. elegans. Specifically, my thesis work aimed to 1) understand how pax-3 expression is regulated in the ventral P cells, focusing on identifying transcription factors that act upstream of pax-3 and activate its expression, 2) better understand the role of PAX-3 in the specification of the P cells, by identifying putative downstream targets of PAX-3, and 3) shed light on regulatory interactions between transcription factors that are required for the specification of ventral hypodermal cell fate.