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

Yi Zhang,Yuhan Gao,Zhonghai Li,Hou-Ling Wang,Hongwei Guo

doi:10.3390/ijms21218120

Abstract

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.

Highlights

Leaves are the primary photosynthetic organs that use the photosynthetic system to fix CO2 to produce carbohydrates, providing energy for plant growth and development [1]
Most of the evidence supporting DNA damage-induced senescence comes from the fact that mutations in genes involved in DNA repair lead to multiple premature aging symptoms, supporting the idea that the balance between DNA damage and repair determines the rate of aging [13]
To further assess whether the expression of ataxia telangiectasia mutated (ATM) mRNA is due to transcriptional regulation, we generated transgenic Arabidopsis plants expressing a GUS (β-glucuronidase) gene driven by the ATM promoter containing a 3 kb fragment upstream of the start codon

Summary

Introduction

Leaves are the primary photosynthetic organs that use the photosynthetic system to fix CO2 to produce carbohydrates, providing energy for plant growth and development [1]. A growing body of evidence indicates that the loss of DNA damage repair induces premature senescence in animals and plants [11,12]. Most of the evidence supporting DNA damage-induced senescence comes from the fact that mutations in genes involved in DNA repair lead to multiple premature aging symptoms, supporting the idea that the balance between DNA damage and repair determines the rate of aging [13]. WRN protein, mutated in Werner syndrome (WS) characterized by premature aging in young adults, is involved in both homologous recombination (HR) and non-homologous end joining (NHEJ) pathways [14]. ATM is activated by auto/transphosphorylation in response to DSBs and leads to the activation of cell cycle checkpoints, DNA repair or apoptosis, while ATR is generally activated by persisting single-stranded DNA breaks (SSBs) [16,19]

Methods

Results

Conclusion