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丝裂原活化蛋白激酶6在水杨酸诱导的叶片衰老过程中调节NPR1基因的表达和激活。

Mitogen-activated protein kinase 6 regulates NPR1 gene expression and activation during leaf senescence induced by salicylic acid.

作者信息

Chai Jinyu, Liu Jian, Zhou Jun, Xing Da

机构信息

MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China.

MOE Key Laboratory of Laser Life Science & Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou 510631, China

出版信息

J Exp Bot. 2014 Dec;65(22):6513-28. doi: 10.1093/jxb/eru369. Epub 2014 Sep 10.

Abstract

Plant senescence is a highly regulated process that can be induced by a range of factors. The nonexpressor of pathogenesis-related genes 1 (npr1) mutant is defective in the salicylic acid (SA) signalling pathway, displaying delayed yellowing during developmental senescence. However, the regulating mechanism of NPR1 on exogenous SA-induced senescence in detached Arabidopsis leaves has not yet been clarified. It was shown here that mitogen-activated protein kinase 6 (MPK6) is involved in promoting exogenous SA-induced detached leaf senescence. During the process of SA-induced senescence, the expression of NPR1 and senescence-related transcription factor WRKY6 was suppressed in mpk6 mutant plants. Further analyses showed that the NPR1 mRNA level is reduced in wrky6 mutants and enhanced in WRKY6 overexpressing lines. Meanwhile, chromatin immunoprecipitation experiments revealed that WRKY6 binds directly to the NPR1 promoter containing W-box motifs. Moreover, inhibition of MPK6 function diminished SA-induced monomerization and nuclear localization of NPR1. In addition, the expression of Trx h5, which catalyses the SA-induced NPR1 activation, was suppressed in the mpk6 mutant, suggesting that MPK6 promotes NPR1 activation, possibly by regulating the expression of Trx h5. Collectively, MPK6-mediated WRKY6 and Trx h5 transcriptional activation co-regulated the expression of the NPR1 gene and the monomerization of NPR1 protein, allowing it to enter the nucleus, thereby promoting SA-induced leaf senescence. These results provide new insight into the mechanism of exogenous SA-induced detached leaf senescence.

摘要

植物衰老过程受到高度调控,可由多种因素诱导。病程相关基因非表达子1(NPR1)突变体在水杨酸(SA)信号通路中存在缺陷,在发育衰老过程中叶片变黄延迟。然而,NPR1对外源SA诱导拟南芥离体叶片衰老的调控机制尚不清楚。本文研究表明,丝裂原活化蛋白激酶6(MPK6)参与促进外源SA诱导的离体叶片衰老。在SA诱导衰老过程中,mpk6突变体植株中NPR1和衰老相关转录因子WRKY6的表达受到抑制。进一步分析表明,wrky6突变体中NPR1 mRNA水平降低,而在WRKY6过表达株系中升高。同时,染色质免疫沉淀实验表明,WRKY6直接结合到含有W盒基序的NPR1启动子上。此外,抑制MPK6功能可减少SA诱导的NPR1单体化和核定位。另外,催化SA诱导NPR1激活的Trx h5在mpk6突变体中的表达受到抑制,这表明MPK6可能通过调节Trx h5的表达来促进NPR1激活。总之,MPK6介导的WRKY6和Trx h5转录激活共同调控NPR1基因的表达和NPR1蛋白的单体化,使其进入细胞核,从而促进SA诱导的叶片衰老。这些结果为外源SA诱导离体叶片衰老的机制提供了新的见解。

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