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Chronic mitochondrial calcium elevation suppresses leaf senescence
- Fu, Shijuan, Li, Luhua, Kang, Huimin, Yang, Xue, Men, Shuzhen, Shen, Yuequan
- Biochemical and biophysical research communications 2017 v.487 pp. 672-677
- Arabidopsis thaliana, calcium, calmodulin, cell death, chlorophyll, hydrogen peroxide, leaves, loss-of-function mutation, mitochondria, mutants
- 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.