SnRK2.4 and SnRK2.10 redundantly control developmental leaf senescence by sustaining ABA production and signaling

Plants constantly and precisely control their growth by inducing distinct developmental programs to survive and produce high-quality offspring in the changing environment. The fine-tuning of the development according to endogenous and environmental signals requires exact intercellular signaling and a balanced response. Kinases of the Sucrose non-fermenting-1-Related protein Kinases type 2 (SnRK2s) family primarily take part in the response and adaptation to environmental stress factors. Notably, here we show that two ABA-non-activated SnRK2s, SnRK2.4 and SnRK2.10, are also activated in non-stress conditions in developmentally senescing leaves of Arabidopsis thaliana . Phenotypic, biochemical, and molecular analyses performed on single snrk2.4 or snrk2.10 , and double snrk2.4/2.10 kinase mutants showed that SnRK2.4 and SnRK2.10, acting redundantly, promote developmental leaf senescence. Further, SnRK2.4 and SnRK2.10 enhance ABA accumulation in senescing leaves by inducing NCED2 , one of key ABA biosynthesis-related genes. The two kinases induce developmental leaf senescence by modulating the expression of multiple ABA-responsive, osmotic stress, and senescence-related genes, such as the senescence master regulators ORE1 , ORS1 , WRKY33, WRKY75, and ANAC087. Furthermore, we show that SnRK2.4 and SnRK2.10 act upstream of MAPK signaling by enhancing the expression and activity of MAPKKK18, a senescence-inducing kinase. These results document a new regulatory function of SnRK2.4 and SnRK2.10: they are activated in Arabidopsis leaves in response to endogenous signals and redundantly induce developmental leaf senescence by stimulating ABA production and sustaining major ABA-dependent and -independent signaling pathways.