Negative feedback control of jasmonate signaling by an alternative splice variant of JAZ10
The plant hormone jasmonate (JA) activates gene expression by promoting ubiquitin-dependent degradation of JAZ transcriptional repressor proteins. A key feature of all JAZ proteins is the highly conserved Jas motif, which mediates both JAZ degradation and JAZ binding to the transcription factor MYC2...
| Autores: | , , , , , , , |
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| Tipo de documento: | artigo |
| Estado: | Versão publicada |
| Data de publicação: | 2013 |
| País: | Argentina |
| Recursos: | Consejo Nacional de Investigaciones Científicas y Técnicas |
| Repositório: | CONICET Digital (CONICET) |
| Idioma: | inglês |
| OAI Identifier: | oai:ri.conicet.gov.ar:11336/23466 |
| Acesso em linha: | http://hdl.handle.net/11336/23466 |
| Access Level: | Acceso aberto |
| Palavra-chave: | JAZ10 SPLICING MYC2 CRYPTIC_DOMAIN https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| Resumo: | The plant hormone jasmonate (JA) activates gene expression by promoting ubiquitin-dependent degradation of JAZ transcriptional repressor proteins. A key feature of all JAZ proteins is the highly conserved Jas motif, which mediates both JAZ degradation and JAZ binding to the transcription factor MYC2. Rapid expression of JAZ genes in response to JA is thought to attenuate JA responses, but little is known about the mechanisms by which newly synthesized JAZ proteins exert repression in the presence of the hormone. Here, we show that desensitization to JA is mediated by an alternative splice variant (JAZ10.4) of JAZ10 that lacks the Jas motif. Unbiased protein-protein interaction screens identified three related bHLH transcription factors (MYC2, MYC3, and MYC4) and the co-repressor NINJA as JAZ10.4-binding partners. We show that the N-terminal region of JAZ10.4 contains a cryptic MYC2-binding site that resembles the Jas motif, and that the ZIM motif of JAZ10.4 functions as a transferable repressor domain whose activity is associated with recruitment of NINJA. Functional studies showed that expression of JAZ10.4 from the native JAZ10 promoter complemented the JA-hypersensitive phenotype of a jaz10 mutant. Moreover, treatment of these complemented lines with JA resulted in rapid accumulation of JAZ10.4 protein. Our results provide an explanation for how the unique domain architecture of JAZ10.4 links transcription factors to a co-repressor complex, and suggest how JA-induced transcription and alternative splicing of JAZ10 pre-mRNA creates a regulatory circuit to attenuate JA responses. |
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