期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 487, 期 3, 页码 672-677出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2017.04.113
关键词
Calcium; Senescence; Calmodulin; BAG protein; Heat-shock protein; Mitochondria
资金
- Ministry of Science and Technology China 973 Program [2013CB910400, 2014CB910201]
- National Natural Science Foundation of China [31570750, 31370826, 31300628, 91017009]
- Tianjin Basic Research Program [14JCQNJ09300, 12JCZDJC23200]
Mitochondria Ca2+ overload has long been recognized as a cell death trigger. Unexpectedly, we demonstrated a signaling complex composed of Calmodulin (CaM), Arabidopsis thaliana Bcl-2-associated athanogene 5 (AtBAG5) and Heat-shock cognate 70 protein (Hsc70) within Arabidopsis thaliana mitochondria which transduces mitochondria Ca2+ elevations to suppress leaf senescence. Gain- and loss-of-function AtBAG5 mutant plants revealed that, mitochondria Ca2+ elevation significantly increase chlorophyll retention and decrease H2O2 level in dark-induced leaf senescence assay. Based on our findings, we proposed a molecular mechanism in which chronic mitochondria Ca2+ elevation reduced ROS levels and thus inhibits leaf senescence. (C) 2017 Elsevier Inc. All rights reserved.
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