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

다국어 초록 (Multilingual 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 MKK5DD 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.










MKK5‐MPK3/6 signaling positively regulates salt tolerance in Arabidopsis, via phosphorylation and degradation of cytokinin signaling components ARR1/10/12.



Salinity stress results in MPK3/6‐mediated phosphorylation and degradation of ARR1/10/12 proteins.

MPK3/6 act upstream of ARR1/10/12 to promote the plant's adaption to high‐salinity.

MPK3/6 are not involved in the regulation of cytokinin signaling under normal growth conditions.


MKK5‐MPK3/6 signaling positively regulates salt tolerance in Arabidopsis, via phosphorylation and degradation of cytokinin signaling components ARR1/10/12.