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Trx CDSP32基因的过表达促进叶绿素合成和光合电子传递,并减轻镉诱导的烟草叶片PSII和PSI的光抑制。

Overexpression of Trx CDSP32 gene promotes chlorophyll synthesis and photosynthetic electron transfer and alleviates cadmium-induced photoinhibition of PSII and PSI in tobacco leaves.

作者信息

Zhang Huihui, Xu Zisong, Huo Yuze, Guo Kaiwen, Wang Yue, He Guoqiang, Sun Hongwei, Li Mabo, Li Xin, Xu Nan, Sun Guangyu

机构信息

College of Resources and Environment, Northeast Agricultural University, Harbin, Heilongjiang, China.

College of Life Science, Northeast Forest University, Harbin, Heilongjiang, China.

出版信息

J Hazard Mater. 2020 Nov 5;398:122899. doi: 10.1016/j.jhazmat.2020.122899. Epub 2020 May 16.

DOI:10.1016/j.jhazmat.2020.122899
PMID:32450465
Abstract

Cadmium stress causes a decrease in chlorophyll content and inhibits photosynthesis in tobacco leaves. The role of thioredoxin-like protein CDSP32 expressed in plant chloroplasts is to alleviates the reduced enzymes expression involved in chlorophyll synthesis of tobacco leaves due to Cd exposure, effectively preventing chlorophyll degradation and promoting increased tobacco biomass. Overexpression of Trx CDSP32 can protect the oxygen-evolving complex on the PSII donor side and promote electron transfer on the PSII acceptor side of tobacco leaves under Cd stress. Trx CDSP32 not only significantly increase the PSI activity of tobacco leaves, but also alleviate cadmium-induced PSI photoinhibition. Although Trx CDSP32 has no significant effect on the expression of PC and FNR proteins in tobacco leaves under Cd stress, it can alleviate the decreased expression of protein subunits involved in photosynthetic electron transfer such as Cyt b6/f complex subunits, Fd, and ATP synthase subunits. Trx CDSP32 can promote the synthesis of chlorophyll, stabilize the electron transfer chain, and promote ATP synthase activity to alleviate cadmium-induced photoinhibition of PSII and PSI in tobacco leaves.

摘要

镉胁迫会导致烟草叶片叶绿素含量降低并抑制光合作用。植物叶绿体中表达的硫氧还蛋白样蛋白CDSP32的作用是缓解因镉暴露导致的烟草叶片叶绿素合成相关酶表达量降低,有效防止叶绿素降解并促进烟草生物量增加。在镉胁迫下,过表达Trx CDSP32可以保护烟草叶片光系统II供体侧的放氧复合体,并促进光系统II受体侧的电子传递。Trx CDSP32不仅显著提高烟草叶片的光系统I活性,还能缓解镉诱导的光系统I光抑制。虽然在镉胁迫下Trx CDSP32对烟草叶片中PC和FNR蛋白的表达没有显著影响,但它可以缓解参与光合电子传递的蛋白亚基如细胞色素b6/f复合体亚基、铁氧还蛋白和ATP合酶亚基的表达量降低。Trx CDSP32可以促进叶绿素合成,稳定电子传递链,并促进ATP合酶活性,以缓解镉诱导的烟草叶片光系统II和光系统I的光抑制。

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