Project description:We report genes induced under transient hypoxia in an ELT-2 dependent manner Adult C. elegans were exposed to transient hypoxia and fed ELT-2 RNAi. Normoxia and Empty Vector RNAi were performed as controls
Project description:ELT-2 is the major transcription factor required for Caenorhabditis elegans intestinal development. It initiates in embryos to promote development then persists after hatching through larval and adult stages. Though the sites of ELT-2 binding are characterized and the transcriptional changes that result from ELT-2 depletion are described, a major missing piece has been the lack of an intestine-specific transcriptome profile over developmental time. We generated this dataset by Fluorescence Activated Cell Sorting (FACS) intestine cells at distinct developmental stages. We analyzed this dataset in conjunction with previously conducted ELT-2 studies to evaluate ELT-2’s role in directing the intestinal regulatory network through development. We found that only 33% of intestine-enriched genes in the embryo were direct targets of ELT-2 but that number increased to 75% by the L3 stage. This suggests additional transcription factors promote intestinal transcription especially in the embryo. Furthermore, only half of ELT-2’s direct target genes were dependent on ELT-2 for their proper expression levels, and an equal proportion of those responded to elt-2 depletion with over-expression as with under-expression. That is, ELT-2 can either activate or repress direct target genes. Indeed, we observed that ELT-2 repressed its own promoter, implicating new models for its autoregulation. Together, our results illustrate that ELT-2 impacts roughly 20 – 50% of intestine-specific genes, that ELT-2 both positively and negatively controls its direct targets, and that our current model of the intestinal regulatory network is incomplete as the factors responsible for directing the expression of many intestinal genes remain unknown.
Project description:Two GATA transcription factors, ELT-2 and ELT-7, function in the differentiation of the Caenorhabditis elegans intestine. Though loss of elt-7 causes no discernable phenotype on its own, it significantly enhances intestinal morphology defects in elt-2 loss-of-function mutants. We sought to identify the cohorts of gene targets unique to or shared by ELT-2 and ELT-7 in an effort to determine the logic underlying their differential impact on intestinal development.