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Formyl tetrahydrofolate deformylase affects hydrogen peroxide accumulation and leaf senescence by regulating the folate status and redox homeostasis in rice

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Science China(Life Sciences) 2021年第5期64卷 720-738页

作者： Erhui Xiong Guojun Dong Fei Chen Chen Zhang Shan Li Yanli Zhang Jahidul Islam Shohag Xiaoe Yang Yihua Zhou Qian Qian Limin Wu Yanchun Yu College of Life and Environmental Sciences Hangzhou Normal UniversityHangzhou 311121China State Key Laboratory for Rice Biology China National Rice Research InstituteHangzhou 310006China Ministry of Education Key Laboratory of Environmental Remediation and Ecosystem Health College of Environmental and Resources ScienceZhejiang UniversityHangzhou 310058China State Key Laboratory of Plant Genomics Institute of Genetics and Developmental BiologyChinese Academy of SciencesBeijing 100101China Laboratory of Rice Biology in Henan Province Collaborative Innovation Center of Henan Grain CropsCollege of AgronomyHenan Agricultural UniversityZhengzhou 450000China

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 ***,we reported a novel rice tetrahydrofolate cycle mutant,which exhibited H_(2)O_(2)accumulation and early leaf senescence ***-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,*** expression of tetrahydrofolate cycle-associated genes encoding serine hydroxymethyl transferase,glycine decarboxylase and 5-formyl tetrahydrofolate cycloligase was significantly *** addition,the accumulation of H_(2)O_(2)in hpa1 was not caused by elevated glycolate *** 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 *** 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 *** 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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Rearrangement of Hydrolysis Products of tetrahydrofolate model compound

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Chinese Chemical Letters 1999年第9期10卷 727-728页

作者： Jian Xin CHENI Jun Sheng HAO Wei GUO Chi Zhong XIA(1Datong Medical College,Datong,Shanxi 0370082Department of Chemistry. Shanxi University, Taiyuan 030006) Datong Medical College Department of Chemistry Shanxi University

The hydrolysis products of tetrahydrofolate model compound 4 were a mixture of 6 and 7 and the rearrangement reaction between 6 and 7 via 5 was in a state of equilibrium, confirmed by (HNMR)-H-1 and IR spectra.

关键词： tetrahydrofolate hydrolysis rearrangement

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Homocysteinemia and methylene tetrahydrofolate reductase gene’s relation to increased risk of coronary artery disease

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外科研究与新技术 2010年第1期19卷 69-74页

作者：艾勒塔夫阿石蒋金法 The Department of Cardiology Tongji Hospital of Tongji University

Objective To review the association of methylene tetrahydrofolate reductase (MTHFR) C677T mutant with coronary artery disease, as well as to highlight the results of some of these studies and to emphasize the need to focus on the genetic architecture of CAD. Data SourcesData used in this article is mainly from relevant articles obtained through Pubmed, OVID and Google Scholar published from 1980 to 2008. Major studies and trials in this period were taken into account to draw accurate conclusion on the relation of those mutations in MTHFR with homocysteinemia and CAD. ResultOur analysis shows that hyperhomocysteinemia, a risk factor for occlusive arterial diseases, can be caused by disruptions of homocysteine metabolism catalyzed by MFTHR. A common alanine to valine mutation in MTHFR may contribute to mild heperhomocysteinemia in CAD. Individuals with the homozygous mutant genotype had higher plasma homocysteine, particularly when plasma folate was below the median value. ConclusionThis MTHFR mutant in the setting of insufficient folate may be a risk factor of CAD and can be regarded as a model of genetic-environmental interaction in the development of CAD.

关键词： methylene tetrahydrofolate reductase polymorphism homocysteinemia folate and coronary artery disease

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