Fu Shijuan, Li Luhua, Kang Huimin, Yang Xue, Men Shuzhen, Shen Yuequan
State Key Laboratory of Medicinal Chemical Biology, Nankai University, 94 Weijin Road, Tianjin 300071, China; College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin 300071, China.
State Key Laboratory of Medicinal Chemical Biology, Nankai University, 94 Weijin Road, Tianjin 300071, China.
Biochem Biophys Res Commun. 2017 Jun 3;487(3):672-677. doi: 10.1016/j.bbrc.2017.04.113. Epub 2017 Apr 24.
Mitochondria Ca 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 Ca elevations to suppress leaf senescence. Gain- and loss-of-function AtBAG5 mutant plants revealed that, mitochondria Ca elevation significantly increase chlorophyll retention and decrease HO level in dark-induced leaf senescence assay. Based on our findings, we proposed a molecular mechanism in which chronic mitochondria Ca elevation reduced ROS levels and thus inhibits leaf senescence.
长期以来，线粒体钙超载一直被认为是细胞死亡的触发因素。出乎意料的是，我们在拟南芥线粒体中发现了一种由钙调蛋白（CaM）、拟南芥Bcl-2相关凋亡诱导基因5（AtBAG5）和热休克同源蛋白70（Hsc70）组成的信号复合物，该复合物可将线粒体钙升高转化为抑制叶片衰老的信号。功能获得和功能丧失的AtBAG5突变体植株表明，在黑暗诱导的叶片衰老试验中，线粒体钙升高显著增加了叶绿素保留量并降低了过氧化氢水平。基于我们的发现，我们提出了一种分子机制，即慢性线粒体钙升高降低了活性氧水平，从而抑制了叶片衰老。
