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Analysis of gene expression changes upon infection of C.elegans with Orsay virus

ABSTRACT: Analysis of the transcriptional response to viral infection in C.elegans.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE41056 | GEO | 2013/06/01

SECONDARY ACCESSION(S): PRJNA175638

REPOSITORIES: GEO

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Analysis of gene expression changes upon infection of C.elegans with Orsay virus

Project description:Analysis of the transcriptional response to viral infection in C.elegans. Comparison of infected and uninfected animals for three strains: N2 (resistant), JU1580 (sensitive), RDE-1 (sensitive)

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Changes in small RNAs upon Viral infection of C.elegans

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Changes in small RNAs upon Viral infection of C.elegans

Project description:Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans Small non-coding RNA (18-30nt) was extracted from animals either infected with Orsay virus or uninfected as indicated.

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Role of STA-1 and SID-3 upon Orsay virus infection in C. elegans (RNA-Seq)

Project description:Across metazoans, innate immunity is vital in defending organisms against viral infection. In mammals, antiviral innate immunity is orchestrated by interferon signaling, activating the STAT transcription factors downstream of the JAK kinases to induce expression of antiviral effector genes. In the nematode C. elegans, which lacks the interferon system, the major antiviral response so far described is RNA interference but whether additional gene expression responses are employed is not known. Here we show that, despite the absence of both interferon and JAK, the C. elegans STAT homologue STA-1 orchestrates antiviral immunity. Intriguingly, mutants lacking STA-1 show increased resistance to antiviral infection. Using gene expression analysis and chromatin immunoprecipitation we show that, in contrast to the mammalian pathway, STA-1 acts as a transcriptional repressor. Thus STA-1 might act to suppress a constitutive antiviral response in the absence of infection. Using a reverse genetic screen we identify the SID-3 as a kinase upstream of STA-1 in the response to infection. Together, our work identifies a novel STAT regulatory cascade controlling its activity in antiviral resistance, illustrating the complex evolutionary trajectory displayed by innate immune signaling pathways across metazoan organisms.

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Role of STA-1 and SID-3 upon Orsay virus infection in C. elegans (ChIP-Seq)

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