ArticlePlant physiology2026
SnRK2.4 and SnRK2.10 redundantly control developmental leaf senescence by sustaining ABA production and signaling.
Article in Plant physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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 nonfermenting-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 2 ABA-nonactivated SnRK2s, SnRK2.4, and SnRK2.10, is also activated in nonstress 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 the key ABA biosynthesis-related genes. The 2 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 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.
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