4.7 Article

An evolutionarily conserved transcriptional response to viral infection in Caenorhabditis nematodes

Journal

BMC GENOMICS
Volume 18, Issue -, Pages -

Publisher

BIOMED CENTRAL LTD
DOI: 10.1186/s12864-017-3689-3

Keywords

Host-virus interaction; Orsay virus; Santeuil virus; N. parisii; C. elegans; C. briggsae; Pathogen infection; Transcriptional profile

Funding

  1. NIH [R21 AI097865]
  2. Burroughs Wellcome Fund

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Background: Caenorhabditis elegans is a powerful model organism for probing many biological processes including host-pathogen interactions with bacteria and fungi. The recent identification of nematode viruses that naturally infect C. elegans and Caenorhabditis briggsae provides a unique opportunity to define host-virus interactions in these model hosts. Results: We analyzed the transcriptional response of pathogen infected C. elegans and C. briggsae by RNA-seq. We identified a total of 320 differentially expressed genes (DEGs) in C. elegans following Orsay virus infection. The DEGs of known function were enriched for ubiquitin ligase related genes; however, the majority of the genes were of unknown function. Interestingly, many DEGs that responded to Orsay virus infection were similar to those induced by Nematocida parisii infection, which is a natural microsporidia pathogen of C. elegans that like Orsay virus infects intestinal cells. Furthermore, comparison of the Orsay virus DEGs in C. elegans to Santeuil virus DEGs in C. briggsae identified 58 C. elegans genes whose orthologs were likewise differentially expressed in C. briggsae, thereby defining an evolutionarily conserved response to viral infection. Conclusions: The two different species C. elegans and C. briggsae, which diverged similar to 18 million years ago, share a common set of transcriptionally responsive genes to viral infection. Furthermore, a subset of these genes were also differentially expressed following infection by a eukaryotic pathogen, N. parisii, suggesting that these genes may constitute a broader pan-microbial response to infection.

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