The endoplasmic reticulum-associated degradation is necessary for plant salt tolerance

被引：127

作者：

Liu, Lijing ^{[1
]}

Cui, Feng ^{[1
]}

Li, Qingliang ^{[1
]}

Yin, Bojiao ^{[1
]}

Zhang, Huawei ^{[1
]}

Lin, Baoying ^{[1
]}

Wu, Yaorong ^{[1
]}

Xia, Ran ^{[1
]}

Tang, Sanyuan ^{[1
]}

Xie, Qi ^{[1
]}

机构：

[1] Chinese Acad Sci, State Key Lab Plant Genom, Natl Ctr Plant Gene Res, Inst Genet & Dev Biol, Beijing 100101, Peoples R China

来源：

CELL RESEARCH | 2011年 / 21卷 / 06期

基金：

中国国家自然科学基金;

关键词：

salt stress; ERAD; UPR; Ca2+; ROS; UNFOLDED PROTEIN RESPONSE; ER-ASSOCIATED DEGRADATION; ARABIDOPSIS-THALIANA; TRANSCRIPTION FACTOR; REACTIVE OXYGEN; STRESS-RESPONSE; QUALITY-CONTROL; ABIOTIC STRESS; SACCHAROMYCES-CEREVISIAE; SIGNAL-TRANSDUCTION;

D O I：

10.1038/cr.2010.181

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Eukaryotic organisms have quality-control mechanisms that allow misfolded or unassembled proteins to be retained in the endoplasmic reticulum (ER) and subsequently degraded by ER-associated degradation (ERAD). The ERAD pathway is well studied in yeast and mammals; however, the biological functions of plant ERAD have not been reported. Through molecular and cellular biological approaches, we found that ERAD is necessary for plants to overcome salt stress. Upon salt treatment ubiquitinated proteins increased in plant cells, especially unfolded proteins that quickly accumulated in the ER and subsequently induced ER stress responses. Defect in HRD3A of the HRD1/HRD3 complex of the ERAD pathway resulted in alteration of the unfolded protein response (UPR), increased plant sensitivity to salt, and retention of ERAD substrates in plant cells. Furthermore, we demonstrated that Ca2+ release from the ER is involved in the elevation of UPR and reactive oxygen species (ROS) participates the ERAD-related plant salt response pathway.

引用

页码：957 / 969

页数：13

共 52 条

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