Project description:RNAi targeting a conserved C. elegans cyclophilin, sig-7, causes defective development and embryonic arrest consistent with a global defect in transcription. The goal of this study was to compare the transcript levels in sig-7(RNAi) embryos to those of L4440/RNAi control embryos to examine the global transcriptional effect caused by of loss of sig-7 function
Project description:RNAi targeting a conserved C. elegans cyclophilin, sig-7, causes defective development and embryonic arrest consistent with a global defect in transcription. The goal of this study was to compare the location of RNA Pol II in sig-7(RNAi) embryos to the localization in L4440/RNAi control embryos to examine the global effect of loss of sig-7 on RNA Pol II regulation and its distribution within gene bodies
Project description:RNAi targeting a conserved C. elegans cyclophilin, sig-7, causes defective development and embryonic arrest consistent with a global defect in transcription. The goal of this study was to compare the transcript levels in sig-7(RNAi) embryos to those of L4440/RNAi control embryos to examine the global transcriptional effect caused by of loss of sig-7 function Examination of RNA levels using RNAseq in 2 replicate samples each of early embryos from sig-7(RNAi) and RNAi controls
Project description:RNAi targeting a conserved C. elegans cyclophilin, sig-7, causes defective development and embryonic arrest consistent with a global defect in transcription. The goal of this study was to compare the location of RNA Pol II in sig-7(RNAi) embryos to the localization in L4440/RNAi control embryos to examine the global effect of loss of sig-7 on RNA Pol II regulation and its distribution within gene bodies anti-AMA-1 ChIP in 2 replicates each of sig-7(RNAi) and RNAi control early stage embryos
Project description:To determine how the genome is packaged in C. elegans sperm, we isolated adult him-8(e1489) males and collected mature sperm (~99% purity). We utilized micrococcal nuclease digestion followed by paired-end sequencing (MNase-seq) to evaluate the presence of nucleosomes across the genome in sperm vs. early embryos. We found that the sperm genome retains nucleosomes genome-wide, comparable to wild-type early embryos.
Project description:Acyl-coA synthases (ACSs) produce fatty acyl-CoAs that are used in metabolic and signaling pathways. Metazoans have a large number of ACS genes with differing expression patterns and substrate preferences, but the physiological roles of most ACS genes are unknown. Here, we focused on the C. elegans acyl CoA synthase, ACS-3, which is known to regulate fat uptake and de novo fat synthesis through the conserved nuclear hormone receptor, nhr-25. We performed microarray analysis of acs-3 mutants to elucidate the acs-3-regulated transcription program. This analysis revealed an enrichment among differentially regulated genes of those involved in lipid metabolism, pathogen and wounding responses, and sterol binding genes, among others. As the immunity genes were the most represented gene class, we performed pathogen sensitivity assays to test the phenotypic consequences of this immune gene regulation. Interestingly, acs-3 mutants were hypersensitive to the fungal pathogen D. coniospora, but only mildly sensitive to the bacterial pathogen P. aeruginosa. acs-3 mutation suppressed nhr-25 mutant sensitivity to P. aeruginosa, yet surprisingly microarray analysis of nhr-25(RNAi) animals revealed significant overlap with the acs-3 mutant transcriptome, with an enrichment of pathogen response genes. The upregulation of pathogen response genes in acs-3(ft5) mutants and following nhr-25 reduction-of-function (rf) does not appear to be due to a constitutive osmotic response or defective cuticle barrier, two potential explanations for the acs-3(ft5) and nhr-25(rf) expression of innate immunity genes in the absence of pathogen exposure. Together, these data indicate that ACS-3 promotes resistance to the fungal pathogen, D. coniospora and regulates innate immunity genes through an unknown mechanism. Potential roles for ACS-3 in innate immunity are discussed.