Although Ca²⁺ has long been recognized as an obligatory intermediate in visual transduction, its role in plant phototransduction remains elusive. Here, we report a Ca²⁺ signaling that controls photoreceptor phyB nuclear translocation in etiolated seedlings during dark-to-light transition. Red light stimulates acute cytosolic Ca²⁺ increases via phyB, which are sensed by Ca²⁺-binding protein kinases, CPK6 and CPK12 (CPK6/12). Upon Ca²⁺ activation, CPK6/12 in turn directly interact with and phosphorylate photo-activated phyB at Ser80/Ser106 to initiate phyB nuclear import. Non-phosphorylatable mutation, phyB^S80A/S106A, abolishes nuclear translocation and fails to complement phyB mutant, which is fully restored by combining phyB^S80A/S106A with a nuclear localization signal. We further show that CPK6/12 function specifically in the early phyB-mediated cotyledon expansion, while Ser80/Ser106 phosphorylation generally governs phyB nuclear translocation. Our results uncover a biochemical regulatory loop centered in phyB phototransduction and provide a paradigm for linking ubiquitous Ca²⁺ increases to specific responses in sensory stimulus processing.

尽管 Ca ²⁺长期以来一直被认为是视觉转导中必不可少的中间体，但它在植物光转导中的作用仍然难以捉摸。在这里，我们报告了一种 Ca ²⁺信号，该信号在暗到亮过渡期间控制黄化幼苗中的光感受器 phyB 核转位。红光通过 phyB 刺激急性细胞溶质 Ca ^{2+增加，这被 Ca 2+}结合蛋白激酶 CPK6 和 CPK12 (CPK6/12)感知。在 Ca ²⁺激活后，CPK6/12 反过来直接与 Ser80/Ser106 处的光激活 phyB 相互作用并磷酸化，以启动 phyB 核输入。非磷酸化突变，phyB ^S80A/S106A，废除核易位并且不能补体phyB突变体，通过结合 phyB ^S80A/S106A和核定位信号完全恢复。我们进一步表明 CPK6/12 在早期 phyB 介导的子叶扩展中具有特异性功能，而 Ser80/Ser106 磷酸化通常控制 phyB 核易位。^{我们的结果揭示了以 phyB 光转导为中心的生化调节回路，并提供了将普遍存在的 Ca 2+}增加与感官刺激处理中的特定反应联系起来的范例。