Chronic mitochondrial calcium elevation suppresses leaf senescence

Abstract

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.

Keywords: BAG protein; Calcium; Calmodulin; Heat-shock protein; Mitochondria; Senescence.