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MPK3/6 诱导的 ARR1/10/12 降解促进拟南芥的耐盐性。

MPK3/6-induced degradation of ARR1/10/12 promotes salt tolerance in Arabidopsis.

机构信息

The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, China.

Development Center of Plant Germplasm Resources, College of Life Sciences, Shanghai Normal University, Shanghai, China.

出版信息

EMBO Rep. 2021 Oct 5;22(10):e52457. doi: 10.15252/embr.202152457. Epub 2021 Aug 17.

Abstract

Cytokinins are phytohormones that regulate plant development, growth, and responses to stress. In particular, cytokinin has been reported to negatively regulate plant adaptation to high salinity; however, the molecular mechanisms that counteract cytokinin signaling and enable salt tolerance are not fully understood. Here, we provide evidence that salt stress induces the degradation of the cytokinin signaling components Arabidopsis (Arabidopisis thaliana) response regulator 1 (ARR1), ARR10 and ARR12. Furthermore, the stress-activated mitogen-activated protein kinase 3 (MPK3) and MPK6 interact with and phosphorylate ARR1/10/12 to promote their degradation in response to salt stress. As expected, salt tolerance is decreased in the mpk3/6 double mutant, but enhanced upon ectopic MPK3/MPK6 activation in an MKK5 line. Importantly, salt hypersensitivity phenotypes of the mpk3/6 line were significantly alleviated by mutation of ARR1/12. The above results indicate that MPK3/6 enhance salt tolerance in part via their negative regulation of ARR1/10/12 protein stability. Thus, our work reveals a new molecular mechanism underlying salt-induced stress adaptation and the inhibition of plant growth, via enhanced degradation of cytokinin signaling components.

摘要

细胞分裂素是一种调节植物发育、生长和应激反应的植物激素。特别是,已有报道称细胞分裂素负调控植物对高盐度的适应;然而,抵消细胞分裂素信号传导并使植物耐受盐度的分子机制尚不完全清楚。在这里,我们提供的证据表明,盐胁迫诱导细胞分裂素信号传导成分拟南芥(Arabidopisis thaliana)反应调节蛋白 1(ARR1)、ARR10 和 ARR12 的降解。此外,应激激活的丝裂原活化蛋白激酶 3(MPK3)和 MPK6 相互作用并磷酸化 ARR1/10/12,以促进它们在盐胁迫下的降解。正如预期的那样,mpk3/6 双突变体的耐盐性降低,但在 MKK5 系中异位激活 MPK3/MPK6 时,耐盐性增强。重要的是,mpk3/6 系的盐敏感表型通过 ARR1/12 的突变得到显著缓解。上述结果表明,MPK3/6 通过负调控 ARR1/10/12 蛋白稳定性在一定程度上增强了植物的耐盐性。因此,我们的工作揭示了一个新的分子机制,即通过增强细胞分裂素信号传导成分的降解,来实现盐诱导的应激适应和抑制植物生长。

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