Department of Energy-Plant Research Laboratory , Michigan State University, East Lansing, Michigan 48824, USA.
Plant Physiol. 2013 Jun;162(2):1006-17. doi: 10.1104/pp.113.218164. Epub 2013 Apr 30.
The plant hormone jasmonate (JA) activates gene expression by promoting ubiquitin-dependent degradation of jasmonate ZIM domain (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 in Arabidopsis (Arabidopsis thaliana) 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 basic helix-loop-helix transcription factors (MYC2, MYC3, and MYC4) and the corepressor NINJA as JAZ10.4-binding partners. We show that the amino-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 the recruitment of NINJA. Functional studies showed that the 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 the 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 corepressor complex and suggest how JA-induced transcription and alternative splicing of JAZ10 premessenger RNA creates a regulatory circuit to attenuate JA responses.
植物激素茉莉酸（JA）通过促进茉莉酸 ZIM 结构域（JAZ）转录阻遏蛋白的泛素依赖性降解来激活基因表达。所有 JAZ 蛋白的一个关键特征是高度保守的 Jas 基序，它介导 JAZ 降解和 JAZ 与转录因子 MYC2 的结合。JAZ 基因对 JA 的快速表达被认为会减弱 JA 反应，但对于新合成的 JAZ 蛋白在激素存在下如何发挥抑制作用的机制知之甚少。在这里，我们在拟南芥（Arabidopsis thaliana）中表明，对 JA 的脱敏是由 JAZ10 的一种替代剪接变体（JAZ10.4）介导的，该变体缺乏 Jas 基序。无偏蛋白-蛋白相互作用筛选鉴定了三个相关的碱性螺旋-环-螺旋转录因子（MYC2、MYC3 和 MYC4）和核心抑因子 NINJA 作为 JAZ10.4 的结合伙伴。我们表明，JAZ10.4 的氨基末端区域包含一个隐藏的 MYC2 结合位点，类似于 Jas 基序，并且 JAZ10.4 的 ZIM 基序作为一个可转移的抑制结构域起作用，其活性与 NINJA 的募集有关。功能研究表明，来自天然 JAZ10 启动子的 JAZ10.4 的表达补充了 jaz10 突变体的 JA 超敏表型。此外，用 JA 处理这些互补系导致 JAZ10.4 蛋白的快速积累。我们的研究结果为 JAZ10.4 的独特结构域架构如何将转录因子与核心抑因子复合物联系起来提供了一个解释，并提出了 JA 诱导的 JAZ10 前体 mRNA 的转录和选择性剪接如何创建一个调节回路来减弱 JA 反应。
