Nitric oxide induces cotyledon senescence involving co-operation of theNES1/MAD1andEIN2-associatedORE1signalling pathways inArabidopsis

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After germination, cotyledons undertake the major role in supplying nutrients to the pre-photoautorophy angiosperm seedlings until they senesce. Like other senescence processes, cotyledon senescence is a programmed degenerative process. Nitric oxide can induce premature cotyledon senescence inArabidopsis thaliana, yet the underlying mechanism remains elusive. A screen for genetic mutants identified thenes1mutant, in which cotyledon senescence was accelerated by nitric oxide. Map-based cloning revealed thatNES1is allelic to a previously reported mitotic checkpoint family gene,MAD1. Thenes1/mad1mutants were restored to the wild type, in response to nitric oxide, by transforming them with pNES1::NES1. Ectopic expression ofNES1in the wild type delayed nitric oxide-mediated cotyledon senescence, confirming the repressive role ofNES1. Moreover, two positive regulators of leaf senescence, the ethylene signalling componentEIN2and the transcription factorORE1/AtNAC2/ANAC092, were found to function during nitric oxide-induced senescence in cotyledons. The block ofORE1function delayed senescence and ectopic expression induced the process, revealing the positive role ofORE1.EIN2was required to induceORE1. Furthermore, the genetic interaction analysis betweenNES1andORE1showed that theore1loss-of-function mutants were epistatic tones1, suggesting the dominant role ofORE1and the antagonistic role ofNES1during nitric oxide-induced cotyledon senescence inArabidopsis.

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