JAZ8 Lacks a Canonical Degron and Has an EAR Motif That Mediates Transcriptional Repression of Jasmonate Responses in Arabidopsis

Abstract

The lipid-derived hormone jasmonoyl-L-Ile (JA-Ile) initiates large-scale changes in gene expression by stabilizing the interaction of JASMONATE ZIM domain (JAZ) repressors with the F-box protein CORONATINE INSENSITIVE1 (COI1), which results in JAZ degradation by the ubiquitin-proteasome pathway. Recent structural studies show that the JAZ1 degradation signal (degron) includes a short conserved LPIAR motif that seals JA-Ile in its binding pocket at the COI1-JAZ interface. Here, we show that Arabidopsis thaliana JAZ8 lacks this motif and thus is unable to associate strongly with COI1 in the presence of JA-Ile. As a consequence, JAZ8 is stabilized against jasmonate (JA)-mediated degradation and, when ectopically expressed in Arabidopsis, represses JA-regulated growth and defense responses. These findings indicate that sequence variation in a hypervariable region of the degron affects JAZ stability and JA-regulated physiological responses. We also show that JAZ8-mediated repression depends on an LxLxL-type EAR (for ERF-associated amphiphilic repression) motif at the JAZ8 N terminus that binds the corepressor TOPLESS and represses transcriptional activation. JAZ8-mediated repression does not require the ZIM domain, which, in other JAZ proteins, recruits TOPLESS through the EAR motifcontaining adaptor protein NINJA. These findings show that EAR repression domains in a subgroup of JAZ proteins repress gene expression through direct recruitment of corepressors to cognate transcription factors.

Arabidopsis MYC Transcription Factors Are the Target of Hormonal Salicylic Acid/Jasmonic Acid Cross Talk in Response to Pieris brassicae Egg Extract

“…JAZ10.4 variant was previously shown to bind to MYC2 but not to COI1, and Arabidopsis plants overexpressing JAZ10.4 exhibited JA-insensitive phenotypes, indicative of a reduced JA signaling pathway (Chung and Howe, 2009). JAZ10.4 and JAZ8, another (Shyu et al, 2012), are thought to constitute a negative feedback loop that prevents exacerbated activation of JA responses. In line with experiments using exogenous application of SA (Van der Does et al, 2013), we conclude that egg-induced SA/JA cross talk is not regulated by increased expression of JAZ10.4 or stabilization of JAZ repressors.…”

A bHLH-Type Transcription Factor, ABA-INDUCIBLE BHLH-TYPE TRANSCRIPTION FACTOR/JA-ASSOCIATED MYC2-LIKE1, Acts as a Repressor to Negatively Regulate Jasmonate Signaling inArabidopsis

“…Molecular mechanisms for attenuating JA signaling were uncovered by identification of JAZ proteins, which negatively regulate JA responses by binding to transcriptional activators, such as MYC2 (Chini et al, 2007;Thines et al, 2007). The existence of degradation-resistant JAZs, including JAZ splice variants, further supports the importance of negative regulation of JA signaling by JAZ proteins (Chung and Howe, 2009;Chung et al, 2010;Shyu et al, 2012). However, JAM1 CRES-T plants exhibit JA-insensitive phenotypes, even when the expression of most of JAZ genes, including JAZ8, was reduced (Figures 2 and 7B) (see Supplemental Figure 17 online).…”

“…Conversely, jaz10 loss-of-function mutants exhibit enhanced JA responses (Yan et al, 2007;Chung and Howe, 2009;Demianski et al, 2012). JAZ8, which lacks a canonical degron and is stabilized against JA-mediated degradation, performs a crucial role in negative regulation of JA signaling (Shyu et al, 2012). The contribution of stable JAZ proteins in restraining JA responses remains unclear, and other mechanisms for negative regulation of JA signaling remain to be discovered.…”

Role of NINJA in root jasmonate signaling

“…It is also possible that more direct mechanisms repress JA-dependent transcription in aerial organs. First, JAZ8 can act independently of NINJA because it carries an ethyleneresponsive element binding factor-associated amphiphilic repression (EAR) motif capable of directly binding TPL (5). This feature is potentially shared by JAZ5, JAZ6, and JAZ7 (32).…”

“…In the current model of JA perception and signaling, JASMONATE ZIM DOMAIN (JAZ) proteins block the function of JA-responsive transcriptional activators in the absence of bioactive JA-Ile (2,3). JAZ proteins form a repressor complex by recruitment of the general corepressor TOPLESS (TPL) and TPL-related proteins either directly or indirectly through interaction with the adaptor protein Novel Interactor of JAZ (NINJA) (4,5). When JA-Ile accumulates, it acts as a bridging ligand between the F-box protein CORONATINE INSENSITIVE 1 (COI1) and JAZ proteins to form the JA coreceptor complex (6).…”