XRN1 Is a Species-Specific Virus Restriction Factor in Yeasts

PLoS Pathogens

Paul A. Rowley¹  Sara L. Sawyer²  Brandon Ho²  Sarah Bushong²  Arlen Johnson² 

[1] BioFrontiers Institute, University of Colorado Boulder, Boulder, Colorado, United States of America;Section of Molecular Biosciences, University of Texas at Austin, Austin, Texas, United States of America

关键词: Saccharomyces cerevisiae;    Fungal evolution;    Viral evolution;    Yeast;    RNA extraction;    Viral replication;    Saccharomyces;    Yeast infections;   

DOI  :  10.1371/journal.ppat.1005890

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

In eukaryotes, the degradation of cellular mRNAs is accomplished by Xrn1 and the cytoplasmic exosome. Because viral RNAs often lack canonical caps or poly-A tails, they can also be vulnerable to degradation by these host exonucleases. Yeast lack sophisticated mechanisms of innate and adaptive immunity, but do use RNA degradation as an antiviral defense mechanism. We find a highly refined, species-specific relationship between Xrn1p and the “L-A” totiviruses of different Saccharomyces yeast species. We show that the gene XRN1 has evolved rapidly under positive natural selection in Saccharomyces yeast, resulting in high levels of Xrn1p protein sequence divergence from one yeast species to the next. We also show that these sequence differences translate to differential interactions with the L-A virus, where Xrn1p from S. cerevisiae is most efficient at controlling the L-A virus that chronically infects S. cerevisiae, and Xrn1p from S. kudriavzevii is most efficient at controlling the L-A-like virus that we have discovered within S. kudriavzevii. All Xrn1p orthologs are equivalent in their interaction with another virus-like parasite, the Ty1 retrotransposon. Thus, Xrn1p appears to co-evolve with totiviruses to maintain its potent antiviral activity and limit viral propagation in Saccharomyces yeasts. We demonstrate that Xrn1p physically interacts with the Gag protein encoded by the L-A virus, suggesting a host-virus interaction that is more complicated than just Xrn1p-mediated nucleolytic digestion of viral RNAs.

【 授权许可】

CC BY