The transient elevation of cytosolic free calcium concentration ([Ca²⁺]_cyt) induced by cold stress is a well‐established phenomenon; however, the underlying mechanism remains elusive. Here, we report that the Ca²⁺‐permeable transporter ANNEXIN1 (AtANN1) mediates cold‐triggered Ca²⁺ influx and freezing tolerance in Arabidopsis thaliana. The loss of function of AtANN1 substantially impaired freezing tolerance, reducing the cold‐induced [Ca²⁺]_cyt 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 Ca²⁺ transport activity, thereby potentiating Ca²⁺ signaling. Consistent with these results and freezing sensitivity of ost1 mutants, the cold‐induced [Ca²⁺]_cyt 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 Ca²⁺ signal generation, which activates the cold response and consequently enhances freezing tolerance in Arabidopsis.

中文翻译：

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钙转运蛋白 ANNEXIN1 介导植物冷诱导的钙信号传导和耐冻性

冷应激引起的细胞溶质游离钙浓度（[Ca ²⁺ ] _{cyt ）的瞬时升高是公认的现象。}然而，潜在的机制仍然难以捉摸。在这里，我们报告了 Ca ²⁺渗透性转运蛋白 ANNEXIN1 (AtANN1) 介导了拟南芥冷触发的 Ca ²⁺流入和耐冻性。AtANN1的功能丧失显着损害了冷冻耐受性，减少了冷诱导的 [Ca ²⁺ ]_{细胞色素增加和冷响应}CBF和COR的上调基因。进一步分析表明，OST1/SnRK2.6 激酶与 AtANN1 相互作用并使其磷酸化，从而增强其 Ca ²⁺转运活性，从而增强 Ca ²⁺信号传导。与这些结果和 ost1 突变体的冷冻敏感性一致，寒冷诱导的ost1-3突变体中的 [Ca ²⁺ ]细胞_色素升高降低。遗传分析表明，AtANN1作用于OST1的下游以响应冷应激。因此，我们的数据揭示了将OST1-AtANN1与冷诱导的 Ca ^{2+联系起来的级联反应}信号产生，激活寒冷反应，从而增强拟南芥的耐寒性。