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Molecular and genetic analyses of GON-14 and other transcriptional regulators of early gonadogenesis in Caenorhabditis elegans

Posted on:2009-10-12Degree:Ph.DType:Dissertation
University:The University of Wisconsin - MadisonCandidate:Chesney, Michael AntonFull Text:PDF
GTID:1440390005453616Subject:Genetics
Abstract/Summary:
The C. elegans distal tip cell (DTC) provides a niche that promotes proliferation of a germline stem cell population. DTC specification requires Wnt signaling, including the POP-1/TCF and SYS-1/beta-catenin transcription factors, and several other factors, including HLH-2/E/Daughterless and GON-14. Here I describe two studies: the molecular and genetic characterization of gon-14 and an investigation of the role of hlh-2 in DTC specification.;The gon-14 locus encodes a putative DNA-binding protein with similarity to LIN-15B, a class B synMuv protein implicated in transcriptional repression. Expression studies and mutant analysis indicate that gon-14 functions in several different tissues during development and promotes larval growth. In addition, genetic analyses link gon-14 to several factors implicated in transcriptional repression and chromatin regulation, including the synMuv genes (e.g. lin-35/Rb) and the mes genes [e.g. mes-2/E(z)]. Furthermore, gon-14 affects expression of pgl-1 and lag-2/Delta, two genes regulated by the synMuv genes. These findings suggest that gon-14 regulates gene expression, perhaps by regulating transcription or chromatin.;HLH-2/E/Da is required for DTC specification in hermaphrodites, but not in males. Strong hlh-2 disruption results in loss of hermaphrodite DTCs, whereas partial hlh-2 loss results in both diminished lag-2/Delta reporter expression and impaired leader cell function. To control DTC specification, hlh-2 genetically interacts with ceh-22/Nkx2-5, a POP-1/TCF target. Ectopic expression studies indicate that hlh-2 is not sufficient for hermaphrodite DTC specification in the absence of Wnt signaling or ceh-22..
Keywords/Search Tags:DTC, Gon-14, Genes, Hlh-2, Expression, Genetic, Transcriptional
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