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HDAC 6 regulates cellular viral RNA sensing by deacetylation of RIG ‐I
Author(s) -
Choi Su Jin,
Lee HyunCheol,
Kim JaeHoon,
Park Song Yi,
Kim TaeHwan,
Lee WoonKyu,
Jang DukJae,
Yoon JiEun,
Choi YoungIl,
Kim Seihwan,
Ma JinYeul,
Kim ChulJoong,
Yao TsoPang,
Jung Jae U,
Lee JooYong,
Lee JongSoo
Publication year - 2016
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201592586
Subject(s) - library science , political science , medicine , computer science
RIG ‐I is a key cytosolic sensor that detects RNA viruses through its C‐terminal region and activates the production of antiviral interferons ( IFN s) and proinflammatory cytokines. While posttranslational modification has been demonstrated to regulate RIG ‐I signaling activity, its significance for the sensing of viral RNA s remains unclear. Here, we first show that the RIG ‐I C‐terminal region undergoes deacetylation to regulate its viral RNA ‐sensing activity and that the HDAC 6‐mediated deacetylation of RIG ‐I is critical for viral RNA detection. HDAC 6 transiently bound to RIG ‐I and removed the lysine 909 acetylation in the presence of viral RNA s, promoting RIG ‐I sensing of viral RNA s. Depletion of HDAC 6 expression led to impaired antiviral responses against RNA viruses, but not against DNA viruses. Consequently, HDAC 6 knockout mice were highly susceptible to RNA virus infections compared to wild‐type mice. These findings underscore the critical role of HDAC 6 in the modulation of the RIG ‐I‐mediated antiviral sensing pathway.