State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing, China.
Institute of Plant Stress Biology, Collaborative Innovation Center of Crop Stress Biology, Henan University, Kaifeng, China.
EMBO J. 2021 Jan 15;40(2):e104559. doi: 10.15252/embj.2020104559. Epub 2020 Dec 29.
The transient elevation of cytosolic free calcium concentration ([Ca ] ) induced by cold stress is a well-established phenomenon; however, the underlying mechanism remains elusive. Here, we report that the Ca -permeable transporter ANNEXIN1 (AtANN1) mediates cold-triggered Ca influx and freezing tolerance in Arabidopsis thaliana. The loss of function of AtANN1 substantially impaired freezing tolerance, reducing the cold-induced [Ca ] increase and upregulation of the cold-responsive CBF and COR genes. Further analysis showed that the OST1/SnRK2.6 kinase interacted with and phosphorylated AtANN1, which consequently enhanced its Ca transport activity, thereby potentiating Ca signaling. Consistent with these results and freezing sensitivity of ost1 mutants, the cold-induced [Ca ] elevation in the ost1-3 mutant was reduced. Genetic analysis indicated that AtANN1 acts downstream of OST1 in responses to cold stress. Our data thus uncover a cascade linking OST1-AtANN1 to cold-induced Ca signal generation, which activates the cold response and consequently enhances freezing tolerance in Arabidopsis.
冷胁迫诱导的细胞质游离钙离子浓度([Ca^2+]i)的短暂升高是一个已被充分证实的现象;然而,其潜在机制仍难以捉摸。在这里,我们报告钙通透性转运蛋白 ANNEXIN1(AtANN1)介导了拟南芥中冷触发的 Ca^2+内流和抗冻性。AtANN1 的功能丧失极大地损害了抗冻性,降低了冷诱导的[Ca^2+]i增加和冷响应的 CBF 和 COR 基因的上调。进一步的分析表明,OST1/SnRK2.6 激酶与 AtANN1 相互作用并磷酸化 AtANN1,从而增强其 Ca^2+转运活性,从而增强 Ca^2+信号。与这些结果和 ost1 突变体的抗冻性一致,ost1-3 突变体中冷诱导的[Ca^2+]i升高减少。遗传分析表明,AtANN1 在响应冷胁迫时位于 OST1 的下游。因此,我们的数据揭示了一个级联反应,将 OST1-AtANN1 与冷诱导的 Ca^2+信号产生联系起来,从而激活冷响应,进而增强拟南芥的抗冻性。