The kinase ATM delays Arabidopsis leaf senescence by stabilizing the phosphatase MKP2 in a phosphorylation-dependent matter.

Abstract

Arabidopsis thaliana (Arabidopsis) Ataxia Telangiectasia Mutated (ATM) kinase plays a vital role in orchestrating leaf senescence; however, the precise mechanisms remain elusive. Here, our study demonstrates that ATM kinase activity is essential for mitigating age- and reactive oxygen species-induced senescence, as restoration of wild-type ATM reverses premature senescence in the atm mutant, while a kinase-dead ATM variant is ineffective. ATM physically interacts with and phosphorylates Mitogen-Activated Protein Kinase Phosphatase 2 (MKP2) to enhance stability under oxidative stress. Mutations in putative phosphorylation sites S15/154 on MKP2 disrupt its phosphorylation, stability, and senescence-delaying function. Moreover, mutation of mitogen-activated protein kinase 6, a downstream target of MKP2, alleviates the premature senescence phenotype of the atm mutant. Notably, the dual specificity protein phosphatase 19 (HsDUSP19), a predicted human counter protein of MPK2, interacts with both ATM and HsATM and extends leaf longevity in Arabidopsis when overexpressed. These findings elucidate the molecular mechanisms underlying the role of ATM in leaf senescence and suggest that the ATM-MKP2 module is likely evolutionarily conserved in regulating the aging process across eukaryotes.