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Onchocerca volvulus is a filarial nematode parasite of humans, causing Onchocerciasis, or River Blindness, which affects over 37 million people, mainly in Africa. It is a severely debilitating disease, which is transmitted to humans by black fly. This project aims to undertake high-throughput sequencing of Onchocerca volvulus transcriptome for de novo assembly of transcripts. The main objective of this project is to recognize genes expressed in given life stages. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see www.sanger.ac.uk/datasharing/

Illumina sequencing of library 3731335, constructed from sample accession ERS092576 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (6970_8). This submission includes reads tagged with the sequence TTAGGCAT.

Illumina sequencing of library 5019066, constructed from sample accession ERS126287 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (7910_6). This submission includes reads tagged with the sequence TAGCTT.

Illumina sequencing of library 3731334, constructed from sample accession ERS092575 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (6970_8). This submission includes reads tagged with the sequence CGATGTTT.

Illumina sequencing of library 5019063, constructed from sample accession ERS126284 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (7910_6). This submission includes reads tagged with the sequence CAGATC.

Illumina sequencing of library 5019065, constructed from sample accession ERS126286 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (7910_6). This submission includes reads tagged with the sequence GATCAG.

Illumina sequencing of library 5019064, constructed from sample accession ERS126285 for study accession ERP001350. This is part of an Illumina multiplexed sequencing run (7910_6). This submission includes reads tagged with the sequence ACTTGA.

GEI-8, a homologue of vertebrate nuclear receptor corepressor NCoR/SMRT, regulates development and neuronal functions in C. elegans.

NCoR and SMRT are two paralogous vertebrate proteins that function as corepressors with unliganded nuclear receptors. Although C. elegans has a large number of nuclear receptors, orthologues of the corepressors NCoR and SMRT have not unambiguously been identified in Drosophila or C. elegans. Here, we identify GEI-8 as the closest homologue of NCoR and SMRT in C. elegans and demonstrate that GEI-8 is expressed as at least two isoforms throughout development in multiple tissues, including neurons, muscle and intestinal cells. We demonstrate that a homozygous deletion within the gei-8 coding region, which is predicted to encode a truncated protein lacking the predicted NR domain, results in severe mutant phenotypes with developmental defects, slow movement and growth, arrested gonadogenesis and defects in cholinergic neurotransmission. Whole genome expression analysis by microarrays identified sets of de-regulated genes consistent with both the observed mutant phenotypes and a role of GEI-8 in regulating transcription. Interestingly, the upregulated transcripts included a predicted mitochondrial sulfide:quinine reductase encoded by Y9C9A.16. This locus also contains non-coding, 21-U RNAs of the piRNA. Inhibition of the expression of the region coding for 21-U RNAs leads to irregular gonadogenesis in the homozygous gei-8 mutants, but not in an otherwise wild-type background, suggesting that GEI-8 may function in concert with the 21-U RNAs to regulate gonadogenesis. Our results confirm that GEI-8 is the orthologue of the vertebrate NCoR/SMRT corepressors and demonstrate important roles for this putative transcriptional corepressor in development and neuronal function.

Microarray expression profiling of C. elegans N2 L4 control (RNAi) vs. nhr-25 (RNAi) and N2 (Wt) vs. acs-3 (ft5) mutants

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.