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Reciprocal inhibition between intracellular antiviral signaling and the RNAi machinery in mammalian cells.

Abstract：

:RNA interference (RNAi) is an established antiviral defense mechanism in plants and invertebrates. Whether RNAi serves a similar function in mammalian cells remains unresolved. We find that in some cell types, mammalian RNAi activity is reduced shortly after viral infection via poly-ADP-ribosylation of the RNA-induced silencing complex (RISC), a core component of RNAi. Well-established antiviral signaling pathways, including RIG-I/MAVS and RNaseL, contribute to inhibition of RISC. In the absence of virus infection, microRNAs repress interferon-stimulated genes (ISGs) associated with cell death and proliferation, thus maintaining homeostasis. Upon detection of intracellular pathogen-associated molecular patterns, RISC activity decreases, contributing to increased expression of ISGs. Our results suggest that, unlike in lower eukaryotes, mammalian RISC is not antiviral in some contexts, but rather RISC has been co-opted to negatively regulate toxic host antiviral effectors via microRNAs.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Seo GJ,Kincaid RP,Phanaksri T,Burke JM,Pare JM,Cox JE,Hsiang TY,Krug RM,Sullivan CS

doi

10.1016/j.chom.2013.09.002

subject

Has Abstract

pub_date

2013-10-16 00:00:00

pages

435-45

issue

4

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(13)00322-3

journal_volume

14

pub_type

杂志文章

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