| Author |
Kalugotla G, Marmerstein V, Schriefer LA, Wang L, Morrison SA, Perez LC, Silverman GA, Schedl T, Pak SC, Baldridge MT.
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| Abstract |
Autophagy is an essential cellular process which functions to maintain homeostasis in response to stressors such as starvation or infection. Here, we report that a subset of autophagy factors including ATG-3 play an antiviral role in Orsay virus infection of Caenorhabditis elegans. Orsay virus infection does not modulate autophagic flux, and re-feeding after starvation limits Orsay virus infection and blocks autophagic flux, suggesting that the role of ATG-3 in Orsay virus susceptibility is independent of its role in maintaining autophagic flux. atg-3 mutants phenocopy rde-1 mutants, which have a defect in RNA interference (RNAi), in susceptibility to Orsay virus infection and transcriptional response to infection. However, atg-3 mutants do not exhibit defects in RNAi. Additionally, ATG-3 limits viral infection at a post-entry step, similar to RDE-1. Differential expression analysis using RNA sequencing revealed that antiviral sqt-2, which encodes a collagen trimer protein, is depleted in mock-infected and infected atg-3 mutants, as well as in infected WT animals, as are numerous other collagen genes. These data suggest that ATG-3 may have a role in collagen organization pathways that function in antiviral defense in C. elegans.
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