Arabidopsis WRKY57 Functions as a Node of Convergence for Jasmonic Acid- and Auxin-Mediated Signaling in Jasmonic Acid-Induced Leaf Senescence
Arabidopsis WRKY57 Functions as a Node of Convergence for Jasmonic Acid- and Auxin-Mediated Signaling in Jasmonic Acid-Induced Leaf Senescence
复制标题
拟南芥 WRKY57 在茉莉酸诱导的叶片衰老中作为茉莉酸和生长素介导的信号传导的汇聚节点
DOI：
10.1105/tpc.113.117838
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发表时间：
2014-01-01
期刊：
影响因子：
11.6
通讯作者：
Yu, Diqiu
中科院分区：
文献类型：
--
作者：
Jiang, Yanjuan;Liang, Gang;Yu, Diqiu
叶片衰老受多种发育和环境因素的调控。外源茉莉酸（JA）能诱导叶片衰老，而生长素抑制这一生理过程。茉莉酸和生长素信号之间的串扰已经得到了很好的研究，但没有在茉莉酸诱导的叶片衰老。在这里，我们发现，茉莉酸甲酯处理后，拟南芥wrky 57突变体产生典型的叶片衰老症状，如变黄的叶片，叶绿素含量低，细胞死亡率高。进一步的研究表明，衰老相关基因在wrky 57突变体中上调。染色质免疫沉淀实验表明WRKY 57可直接与衰老相关基因SENESCENCE 4和SENESCENCE-ASSOCIATED GENE 12的启动子结合并抑制其转录。体内和体外实验表明，WRKY 57与JASMONATE ZIM-DOMAIN 4/8（JAZ 4/8）和AUX/IAA蛋白IAA 29相互作用，它们分别是JA和生长素信号传导途径的阻遏物。与JA和生长素在JA诱导的叶片衰老中的相反功能相一致，JAZ 4/8和IAA 29在JA诱导的叶片衰老中也显示出相反的功能，并且与WRKY 57竞争性地相互作用。我们的研究结果表明，生长素可以通过WRKY 57拮抗茉莉酸诱导的叶片衰老过程。此外，WRKY 57蛋白水平被JA下调，但被生长素上调。因此，WRKY 57作为JA诱导的叶片衰老的阻遏物，是JA和生长素介导的信号通路的共同组分。
Leaf senescence is regulated by diverse developmental and environmental factors. Exogenous jasmonic acid (JA) can induce leaf senescence, whereas auxin suppresses this physiological process. Crosstalk between JA and auxin signaling has been well studied, but not during JA-induced leaf senescence. Here, we found that upon methyl jasmonate treatment, Arabidopsis thaliana wrky57 mutants produced typical leaf senescence symptoms, such as yellowing leaves, low chlorophyll content, and high cell death rates. Further investigation suggested that senescence-associated genes were upregulated in the wrky57 mutants. Chromatin immunoprecipitation experiments revealed thatWRKY57 directly binds to the promoters of SENESCENCE4 and SENESCENCE-ASSOCIATED GENE12 and represses their transcription. In vivo and in vitro experiments suggested that WRKY57 interacts with JASMONATE ZIM-DOMAIN4/8 (JAZ4/8) and the AUX/IAA protein IAA29, repressors of the JA and auxin signaling pathways, respectively. Consistent with the opposing functions of JA and auxin in JA-induced leaf senescence, JAZ4/8 and IAA29 also displayed opposite functions in JA-induced leaf senescence and competitively interacted with WRKY57. Our results suggested that the JA-induced leaf senescence process can be antagonized by auxin viaWRKY57. Moreover, WRKY57 protein levels were downregulated by JA but upregulated by auxin. Therefore, as a repressor in JA-induced leaf senescence, WRKY57 is a common component of the JA- and auxin-mediated signaling pathways.