Jasmonate (JA) is a lipid-derived phytohormone that regulates a broad range of physiological processes, including wound responses, defense against insect herbivores and pathogens, and plant growth and development. JASMONATE ZIM-DOMAIN (JAZ) proteins are negative regulators of transcription factors that repress JA-induced gene expression. The current JA signaling model indicates that JAZ proteins require the adaptor protein NOVEL INTERACTOR OF JAZ (NINJA) to recruit the co-repressor TOPLESS (TPL) and repress transcription of JA-response genes. Upon wounding or other biological cues that lead to accumulation of bioactive JA, JAZ proteins are targeted for ubiquitination by the F-box protein CORONATINE INSENSITIVE1 (COI1) and degraded by the 26S proteasome. Degradation of JAZ proteins results in induction of JA-responsive gene expression. There are 12 JAZ proteins in Arabidopsis, and it is unknown how they regulate such a wide range of biological processes. In this study, I first show that JAZ proteins exhibit differential stability upon JA treatment, with JAZ8 being a relatively stable repressor. The increased stability of JAZ8 is a consequence of a unique degron motif that differs from the canonical degron of most others JAZs. Secondly, I report that JAZ8 represses JA-induced gene expression through its N-terminal EAR (for EAR-associated amphiphilic repression) motif, and that the EAR motif is required for direct interaction of JAZ8 with TPL. This finding suggests that JAZ8 does not repress JA responses through NINJA. Finally, I report the identification of a novel JAZ protein (called JAZ13) in Arabidopsis that is most closely related to JAZ7 and JAZ8. I provide genetic and biochemical evidence that JAZ13, like JAZ8, negatively regulates JA responses through a NINJA-independent pathway. Taken together, results from this study elucidate a novel mechanism to recruit TPL and repress JA responses, presumably for the purpose of fine-tuning myriad JA responses that balance plant defense and development.
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