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Negative feedback regulation of RIG-1-mediated antiviral signaling by interferon-induced ISG15 conjugation

Title
Negative feedback regulation of RIG-1-mediated antiviral signaling by interferon-induced ISG15 conjugation
Authors
Kim, MJHwang, SYImaizumi, TYoo, JY
POSTECH Authors
Yoo, JY
Date Issued
Feb-2008
Publisher
AMER SOC MICROBIOLOGY
Abstract
RIG-I senses intracellular virus-specific nucleic acid structures and initiates an antiviral response that induces interferon (IFN) production, which, in turn, activates the transcription of RIG-I to increase RIG-I protein levels. Upon intracellular poly(I:C) stimulation, however, the levels of RIG-I protein did not correlate with the expression patterns of RIG-I transcripts. When the ISG15 conjugation system was overexpressed, ISG15 was conjugated to RIG-I and cellular levels of the unconjugated form of RIG-I decreased. The ISGylation of RIG-I reduced levels of both basal and virus-induced IFN promoter activity. Levels of unconjugated RIG-I also decreased when 26S proteasome activity was blocked by treatment with MG132, ALLN, or Lactacystin. In the presence of MG132, ISGI5 conjugation to RIG-I increased, and hence, the unconjugated form of RIG-I was reduced. In Ube1L(-/-) cells, which lack the ability to conjugate ISG15, basal levels of both RIG-I protein and transcripts were increased compared to those in wild-type cells. As a result, enhanced production of ISGs and enhanced IFN promoter activity in Ube1L(-/-) cells were observed, and the phenotype was restored to that of wild-type cells by the overexpression of Ube1L. Based on these results, we propose a novel negative feedback loop which adjusts the strength of the RIG-I-mediated antiviral response and IFN production through the regulation of RIG-I protein by IFN-induced ISG15 conjugation.
URI
http://oasis.postech.ac.kr/handle/2014.oak/11313
DOI
10.1128/JVI.01650-07
ISSN
0022-538X
Article Type
Article
Citation
JOURNAL OF VIROLOGY, vol. 82, no. 3, page. 1474 - 1483, 2008-02
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유주연YOO, JOO YEON
Dept of Life Sciences
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