The alg-1 Gene Is Necessary for Orsay Virus Replication in Caenorhabditis elegans

Ciro Cubillas, Luis Enrique Sandoval Del Prado, Sydney Goldacker, Chika Fujii, Amanda N. Pinski, Jon Zielke, David Wang

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

The establishment of the Orsay virus-Caenorhabditis elegans infection model has enabled the identification of host factors essential for virus infection. Argonautes are RNA interacting proteins evolutionary conserved in the three domains of life that are key components of small RNA pathways. C. elegans encodes 27 argonautes or argonaute-like proteins. Here, we determined that mutation of the argonaute-like gene 1, alg-1, results in a greater than 10,000-fold reduction in Orsay viral RNA levels, which could be rescued by ectopic expression of alg-1. Mutation in ain-1, a known interactor of ALG-1 and component of the RNA-induced silencing complex, also resulted in a significant reduction in Orsay virus levels. Viral RNA replication from an endogenous transgene replicon system was impaired by the lack of ALG-1, suggesting that ALG-1 plays a role during the replication stage of the virus life cycle. Orsay virus RNA levels were unaffected by mutations in the ALG-1 RNase H-like motif that ablate the slicer activity of ALG-1. These findings demonstrate a novel function of ALG-1 in promoting Orsay virus replication in C. elegans.

Original languageEnglish
JournalJournal of virology
Volume97
Issue number4
DOIs
StatePublished - Apr 2023

Keywords

  • Aargonaute
  • Caenorhabditis elegans
  • Orsay virus
  • RISC
  • alg-1
  • alg-2

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