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^DD 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.

中文翻译：

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MPK3/6 诱导的 ARR1/10/12 降解促进拟南芥耐盐性

细胞分裂素是调节植物发育、生长和对压力的反应的植物激素。特别是，据报道，细胞分裂素可负调节植物对高盐度的适应。然而，抵消细胞分裂素信号传导和使耐盐性成为可能的分子机制尚不完全清楚。在这里，我们提供了盐胁迫诱导细胞分裂素信号成分拟南芥( Arabidopisis thaliana ) 响应调节因子 1 (ARR1)、ARR10 和 ARR12 降解的证据。此外，应激激活的丝裂原激活蛋白激酶 3 (MPK3) 和 MPK6 与 ARR1/10/12 相互作用并使其磷酸化，以促进其在盐胁迫下的降解。正如预期的那样， mpk3 / 6中的耐盐性降低双突变体，但在MKK5 ^DD系中的异位 MPK3/MPK6 激活后增强。重要的是，通过 ARR1/12 的突变显着减轻了mpk3 / 6系的盐过敏表型。上述结果表明，MPK3/6 部分通过其对 ARR1/10/12 蛋白稳定性的负调节来增强耐盐性。因此，我们的工作通过增强细胞分裂素信号成分的降解，揭示了盐诱导的胁迫适应和植物生长抑制的新分子机制。