机构地区:[1]College of Life and Environmental Sciences,Hangzhou Normal University,Hangzhou 311121,China [2]State Key Laboratory for Rice Biology,China National Rice Research Institute,Hangzhou 310006,China [3]Ministry of Education Key Laboratory of Environmental Remediation and Ecosystem Health,College of Environmental and Resources Science,Zhejiang University,Hangzhou 310058,China [4]State Key Laboratory of Plant Genomics,Institute of Genetics and Developmental Biology,Chinese Academy of Sciences,Beijing 100101,China [5]Laboratory of Rice Biology in Henan Province,Collaborative Innovation Center of Henan Grain Crops,College of Agronomy,Henan Agricultural University,Zhengzhou 450000,China
出 处:《Science China(Life Sciences)》2021年第5期720-738,共19页中国科学(生命科学英文版)
基 金:the National Key Research and Development Program of China(2016YFD0101801);the National Natural Science Foundation of China(91735303 and 91335103);the Natural Science Foundation of Zhejiang(LY18C130010,LY18C130009,and LY20C130004);the Science and Technology Project of Hangzhou(20180432B03,20180432B09,and 20180432B04);the Foundation of Zhejiang Education Department(Y201431296)。
摘 要:It is well established that an abnormal tetrahydrofolate(THF)cycle causes the accumulation of hydrogen peroxide(H_(2)O_(2))and leaf senescence,however,the molecular mechanism underlying this relationship remains largely unknown.Here,we reported a novel rice tetrahydrofolate cycle mutant,which exhibited H_(2)O_(2)accumulation and early leaf senescence phenotypes.Map-based cloning revealed that HPA1 encodes a tetrahydrofolate deformylase,and its deficiency led to the accumulation of tetrahydrofolate,5-formyl tetrahydrofolate and 10-formyl tetrahydrofolate,in contrast,a decrease in 5,10-methenyl-tetrahydrofolate.The expression of tetrahydrofolate cycle-associated genes encoding serine hydroxymethyl transferase,glycine decarboxylase and 5-formyl tetrahydrofolate cycloligase was significantly down-regulated.In addition,the accumulation of H_(2)O_(2)in hpa1 was not caused by elevated glycolate oxidation.Proteomics and enzyme activity analyses further revealed that mitochondria oxidative phosphorylation complex I and complex V were differentially expressed in hpa1,which was consistent with the H_(2)O_(2)accumulation in hpa1.In a further feeding assay with exogenous glutathione(GSH),a non-enzymatic antioxidant that consumes H_(2)O_(2),the H_(2)O_(2)accumulation and leaf senescence phenotypes of hpa1 were obviously compensated.Taken together,our findings suggest that the accumulation of H_(2)O_(2)in hpa1 may be mediated by an altered folate status and redox homeostasis,subsequently triggering leaf senescence.
关 键 词:H_(2)O_(2) leaf senescence TETRAHYDROFOLATE oxidative phosphorylation GSH programmed cell death
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