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Repression of jasmonate signaling by a non‐TIFY JAZ protein in Arabidopsis
Author(s) -
Thireault Caitlin,
Shyu Christine,
Yoshida Yuki,
St. Aubin Brian,
Campos Marcelo L.,
Howe Gregg A.
Publication year - 2015
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12841
Subject(s) - repressor , jasmonate , arabidopsis , biology , transcription factor , psychological repression , gene , mutant , genetics , transcription (linguistics) , microbiology and biotechnology , gene expression , linguistics , philosophy
Summary JAsmonate ZIM‐domain (JAZ) proteins repress the activity of transcription factors that execute responses to the plant hormone jasmonoyl‐L‐isoleucine (JA‐Ile). The ZIM protein domain recruits the co‐repressors NINJA and TOPLESS to JAZ‐bound transcription factors, and contains a highly conserved TIF[F/Y]XG motif that defines the larger family of TIFY proteins to which JAZs belong. Here, we report that diverse plant species contain genes encoding putative non‐TIFY JAZ proteins, including a previously unrecognized JAZ repressor in Arabidopsis (JAZ13, encoded by At3g22275). JAZ13 is most closely related to JAZ8 and includes divergent EAR, TIFY/ZIM, and Jas motifs. Unlike JAZ8, however, JAZ13 contains a Ser‐rich C‐terminal tail that is a site for phosphorylation. Overexpression of JAZ13 resulted in reduced sensitivity to JA, attenuation of wound‐induced expression of JA‐response genes, and decreased resistance to insect herbivory. JAZ13 interacts with the bHLH transcription factor MYC2 and the co‐repressor TOPLESS but, consistent with the absence of a TIFY motif, neither NINJA nor other JAZs. Analysis of single and higher‐order T‐DNA insertion jaz null mutants provided further evidence that JAZ13 is a repressor JA signaling. Our results demonstrate that proteins outside the TIFY family are functional JAZ repressors and further suggest that this expansion of the JAZ family allows fine‐tuning of JA‐mediated transcriptional responses.