Melatonin delays ABA-induced leaf senescence via H 2 O 2 -dependent calcium signalling.

Precocious leaf senescence can reduce crop yield and quality by limiting the growth stage. Melatonin has been shown to delay leaf senescence; however, the underlying mechanism remains obscure. Here, we show that melatonin offsets abscisic acid (ABA) to protect photosystem II and delay the senescence of attached old leaves under the light. Melatonin induced H 2 O 2 accumulation accompanied by an upregulation of melon respiratory burst oxidase homolog D (CmRBOHD) under ABA-induced stress. Both melatonin and H 2 O 2 induced the accumulation of cytoplasmic-free Ca 2+ ([Ca 2+ ] cyt ) in response to ABA, while blocking of Ca 2+ influx channels attenuated melatonin- and H 2 O 2 -induced ABA tolerance. CmRBOHD overexpression induced [Ca 2+ ] cyt accumulation and delayed leaf senescence, whereas deletion of Arabidopsis AtRBOHD, a homologous gene of CmRBOHD, compromised the melatonin-induced [Ca 2+ ] cyt accumulation and delay of leaf senescence in Arabidopsis under ABA stress. Furthermore, melatonin, H 2 O 2  and Ca 2+ attenuated ABA-induced K + efflux and subsequent cell death. CmRBOHD overexpression and AtRBOHD deletion alleviated and aggravated the ABA-induced K + efflux, respectively. Taken together, our study unveils a new mechanism by which melatonin offsets ABA action to delay leaf senescence via RBOHD-dependent H 2 O 2 production that triggers [Ca 2+ ] cyt accumulation and subsequently inhibits K + efflux and delays cell death/leaf senescence in response to ABA.