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Leaf senescence is the final stage of leaf development. It is accompanied by the remobilization of nutrients from senescent leaves to developing organs. The occurrence of senescence is the consequence of integrating intrinsic and environmental signals. DNA damage triggered by stresses has been regarded as one of the reasons for senescence. To prevent DNA damage, cells have evolved elaborate DNA repair machinery. The ataxia telangiectasia mutated (ATM) functions as the chief transducer of the double-strand breaks (DSBs) signal. Our previous study suggests that ATM functions in lifespan regulation in Arabidopsis . However, ATM regulatory mechanism on plant longevity remains unclear. Here, we performed chemical mutagenesis to identify the components involved in ATM-mediated longevity and obtained three dominant mutants satmf1~3 , suppressor of atm in fertility , displaying delayed senescence and restored fertility in comparison with atm mutant. Molecular cloning and functional analysis of SATMF (suppressor of atm in fertility) will help to understand the underlying regulatory mechanism of ATM in plants, and shed light on developing new treatments for the disease Ataxia-telangiectasia.

SATMF Suppresses the Premature Senescence Phenotype of the ATM Loss-of-Function Mutant and Improves Its Fertility in Arabidopsis