iTRAQ-based proteomic analysis provides insights into the molecular mechanisms of rice formyl tetrahydrofolate deformylase in salt response

文献类型： 外文期刊

第一作者： Xiong, Erhui

作者： Xiong, Erhui;Zhang, Chen;Ye, Chenxi;Jiang, Yaohuang;Zhang, Yanli;Chen, Fei;Yu, Yanchun;Wu, Limin;Dong, Guojun;Zeng, Dali

作者机构：

关键词： Chloroplast; Energy metabolism; Electron transport chain; Mitochondrial; Reactive oxygen species

期刊名称：PLANTA （ 影响因子：4.116； 五年影响因子：4.316 ）

ISSN： 0032-0935

年卷期： 2021 年 254 卷 4 期

页码：

收录情况： SCI

摘要： Main conclusion A new molecular mechanism of tetrahydrofolate deformylase involved in the salt response presumably affects mitochondrial and chloroplast function by regulating energy metabolism and accumulation of reactive oxygen species. High salinity severely restrains plant growth and development, consequently leading to a reduction in grain yield. It is therefore critical to identify the components involved in plant salt resistance. In our previous study, we identified a rice leaf early-senescence mutant hpa1, which encodes a formyl tetrahydrofolate deformylase (Xiong et al. in Sci China Life Sci 64(5):720-738, 2021). Here, we report that HPA1 also plays a role in the salt response. To explore the molecular mechanism of HPA1 in salt resistance, we attempted to identify the differentially expressed proteins between wild type and hpa1 mutant for salinity treatment using an iTRAQ-based comparative protein quantification approach. A total of 4598 proteins were identified, of which 279 were significantly altered, including 177 up- and 102 down-regulated proteins. A functional analysis suggested that the 279 differentially expressed proteins are involved mainly in the regulation of oxidative phosphorylation, phenylpropanoid biosynthesis, photosynthesis, posttranslational modifications, protein turnover and energy metabolism. Moreover, a deficiency in HPA1 impaired chlorophyll metabolism and photosynthesis in chloroplasts and affected the electron flow of the electron transport chain in mitochondria. These changes led to abnormal energy metabolism and accumulation of reactive oxygen species, which may affect the permeability and integrity of cell membranes, leading to cell death. In addition, the results were verified by transcriptional or physiological experiments. Our results provide an insight into a new molecular mechanism of the tetrahydrofolate cycle protein formyl tetrahydrofolate deformylase, which is involved in the salt response, presumably by affecting mitochondrial and chloroplast function regulating energy metabolism and accumulation of reactive oxygen species under salt stress.

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