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The C. elegans RIG-I homolog drh-1 mediates the Intracellular Pathogen Response upon viral infection

By Jessica N. Sowa, Hongbing Jiang, Lakshmi Somasundaram, Guorong Xu, David Wang, Emily R. Troemel

Posted 18 Jul 2019
bioRxiv DOI: 10.1101/707141 (published DOI: 10.1128/JVI.01173-19)

Mammalian RIG-I-like receptors detect viral dsRNA and 5′ triphosphorylated RNA to activate transcription of interferon genes and promote antiviral defense. The C. elegans RIG-I-like receptor DRH-1 promotes defense through antiviral RNA interference, but less is known about its role in regulating transcription. Here we describe a role for drh-1 in directing a transcriptional response in C. elegans called the Intracellular Pathogen Response (IPR), which is associated with increased pathogen resistance. The IPR includes a set of genes induced by diverse stimuli including intracellular infection and proteotoxic stress. Previous work suggested that the proteotoxic stress caused by intracellular infections might be the common trigger of the IPR, but here we demonstrate that different stimuli act through distinct pathways. Specifically, we demonstrate that DRH-1/RIG-I is required for inducing the IPR in response to Orsay virus infection, but not in response to other triggers like microsporidian infection or proteotoxic stress. Furthermore, drh-1 appears to be acting independently of its known role in RNAi. Interestingly, expression of the replication competent Orsay virus RNA1 segment alone is sufficient to induce most of the IPR genes in a manner dependent on RNA dependent RNA polymerase activity and on drh-1 . Altogether, these results suggest that DRH-1 is a pattern-recognition receptor that detects viral replication products to activate the IPR stress/immune program in C. elegans .

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