Tobacco calmodulin-like protein provides secondary defense by binding to and directing degradation of virus RNA silencing suppressors

Kenji S. Nakahara*, Chikara Masuta, Syouta Yamada, Hanako Shimura, Yukiko Kashihara, Tomoko S. Wada, Ayano Meguro, Kazunori Goto, Kazuki Tadamura, Kae Sueda, Toru Sekiguchi, Jun Shao, Noriko Itchoda, Takeshi Matsumura, Manabu Igarashi, Kimihito Ito, Richard W. Carthew, Ichiro Uyeda

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

109 Scopus citations

Abstract

RNA silencing (RNAi) induced by virus-derived double-stranded RNA (dsRNA), which is in a sense regarded as a pathogen-associated molecular pattern (PAMP) of viruses, is a general plant defense mechanism. To counteract this defense, plant viruses express RNA silencing suppressors (RSSs), many of which bind to dsRNA and attenuate RNAi. We showed that the tobacco calmodulin-like protein, rgs-CaM, counterattacked viral RSSs by binding to their dsRNA-binding domains and sequestering them from inhibiting RNAi. Autophagy-like protein degradation seemed to operate to degrade RSSs with the sacrifice of rgs-CaM. These RSSs could thus be regarded as secondary viral PAMPs. This study uncovered a unique defense system in which an rgs-CaM-mediated countermeasure against viral RSSs enhanced host antiviral RNAi in tobacco.

Original languageEnglish (US)
Pages (from-to)10113-10118
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume109
Issue number25
DOIs
StatePublished - Jun 19 2012

Keywords

  • Arms race
  • Innate immunity
  • Ubiquitin-26S proteasome

ASJC Scopus subject areas

  • General

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