Phosphorylation of Thr-225 and Ser-262 on ERD7 Promotes Age-Dependent and Stress-Induced Leaf Senescence through the Regulation of Hydrogen Peroxide Accumulation in Arabidopsis thaliana
文献类型: 外文期刊
第一作者: Wu, Rongrong
作者: Wu, Rongrong;Wu, Rongrong;Pan, Xiaolu;Li, Wei;Zhang, Zenglin;Guo, Yongfeng
作者机构:
关键词: ERD7; leaf senescence; phosphorylation; ROS; Arabidopsis thaliana
期刊名称:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ( 影响因子:5.6; 五年影响因子:6.2 )
ISSN: 1661-6596
年卷期: 2024 年 25 卷 2 期
页码:
收录情况: SCI
摘要: As the final stage of leaf development, leaf senescence is affected by a variety of internal and external signals including age and environmental stresses. Although significant progress has been made in elucidating the mechanisms of age-dependent leaf senescence, it is not clear how stress conditions induce a similar process. Here, we report the roles of a stress-responsive and senescence-induced gene, ERD7 (EARLY RESPONSIVE TO DEHYDRATION 7), in regulating both age-dependent and stress-induced leaf senescence in Arabidopsis. The results showed that the leaves of erd7 mutant exhibited a significant delay in both age-dependent and stress-induced senescence, while transgenic plants overexpressing the gene exhibited an obvious accelerated leaf senescence. Furthermore, based on the results of LC-MS/MS and PRM quantitative analyses, we selected two phosphorylation sites, Thr-225 and Ser-262, which have a higher abundance during senescence, and demonstrated that they play a key role in the function of ERD7 in regulating senescence. Transgenic plants overexpressing the phospho-mimetic mutant of the activation segment residues ERD7(T225D) and ERD7(T262D) exhibited a significantly early senescence, while the inactivation segment ERD7(T225A) and ERD7(T262A) displayed a delayed senescence. Moreover, we found that ERD7 regulates ROS accumulation by enhancing the expression of AtrbohD and AtrbohF, which is dependent on the critical residues, i.e., Thr-225 and Ser-262. Our findings suggest that ERD7 is a positive regulator of senescence, which might function as a crosstalk hub between age-dependent and stress-induced leaf senescence.
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