Abstract
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 in Arabidopsis thaliana, yet the underlying mechanism remains elusive. A screen for genetic mutants identified the nes1 mutant, in which cotyledon senescence was accelerated by nitric oxide. Map-based cloning revealed that NES1 is allelic to a previously reported mitotic checkpoint family gene, MAD1. The nes1/mad1 mutants were restored to the wild type, in response to nitric oxide, by transforming them with pNES1::NES1. Ectopic expression of NES1 in the wild type delayed nitric oxide-mediated cotyledon senescence, confirming the repressive role of NES1. Moreover, two positive regulators of leaf senescence, the ethylene signalling component EIN2 and the transcription factor ORE1/AtNAC2/ANAC092, were found to function during nitric oxide-induced senescence in cotyledons. The block of ORE1 function delayed senescence and ectopic expression induced the process, revealing the positive role of ORE1. EIN2 was required to induce ORE1. Furthermore, the genetic interaction analysis between NES1 and ORE1 showed that the ore1 loss-of-function mutants were epistatic to nes1, suggesting the dominant role of ORE1 and the antagonistic role of NES1 during nitric oxide-induced cotyledon senescence in Arabidopsis.
Highlights
Mutagenized, light-grown seedlings were screened for enhanced cotyledon senescence in response to treatment with nitric oxide, and a line, named nes1-6, was isolated
Cotyledon senescence leads to various alterations in the physiological homeostasis of plants, which can result in plant seedlings failing to initiate and cause agricultural losses (Zhou and Brown, 2006; Chandler, 2008), but the molecular mechanism of cotyledon senescence is currently uncertain
The phenotype of nitric oxideinduced cotyledon senescence was investigated and the nes1 mutant was characterized as having early cotyledon senescence which was induced by nitric oxide
Summary
As an integral part of development, the senescence of cotyledons is a process that leads to nutrient recycling and ends in cell death, and is accompanied by colour changes, the dismantling of chloroplasts, and the degradation of DNA, RNA, and protein (Krul, 1974; Peterman and Siedow, 1985). Phytohormones such as cytokinin and ethylene affect cotyledon senescence, with cytokinin preventing chlorophyll breakdown and ethylene initiating the onset of the senescence process (Ananieva et al, 2008a; Jing et al, 2008). Cotyledon senescence has been studied for decades (McKersie et al, 1987; Rukes and Mulkey, 1993), its underlying regulatory network is unclear
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