Early plant responses to different stress situations often encompass cytosolic Ca²⁺ increases, plasma membrane depolarization and the generation of reactive oxygen species^1,2,3. However, the mechanisms by which these signalling elements are translated into defined physiological outcomes are poorly understood. Here, to study the basis for encoding of specificity in plant signal processing, we used light-gated ion channels (channelrhodopsins). We developed a genetically engineered channelrhodopsin variant called XXM 2.0 with high Ca²⁺ conductance that enabled triggering cytosolic Ca²⁺ elevations in planta. Plant responses to light-induced Ca²⁺ influx through XXM 2.0 were studied side by side with effects caused by an anion efflux through the light-gated anion channelrhodopsin ACR1 2.0⁴. Although both tools triggered membrane depolarizations, their activation led to distinct plant stress responses: XXM 2.0-induced Ca²⁺ signals stimulated production of reactive oxygen species and defence mechanisms; ACR1 2.0-mediated anion efflux triggered drought stress responses. Our findings imply that discrete Ca²⁺ signals and anion efflux serve as triggers for specific metabolic and transcriptional reprogramming enabling plants to adapt to particular stress situations. Our optogenetics approach unveiled that within plant leaves, distinct physiological responses are triggered by specific ion fluxes, which are accompanied by similar electrical signals.

植物对不同胁迫情况的早期反应通常包括胞质 Ca²⁺ 增加、质膜去极化和活性氧的产生^1,2,3。然而，这些信号元件转化为确定的生理结果的机制知之甚少。在这里，为了研究植物信号处理中特异性编码的基础，我们使用了光门控离子通道 （通道视紫红质）。我们开发了一种名为 XXM 2.0 的基因工程通道视紫红质变体，具有高 Ca²⁺ 电导率，能够触发植物中胞质 Ca²⁺ 升高。并排研究了植物对通过 XXM 2.0 光诱导的 Ca²⁺ 内流的响应，以及阴离子通过光门控阴离子通道视紫红质 ACR1 2.0 4 外流引起的^影响。尽管这两种工具都触发了膜去极化，但它们的激活导致了不同的植物胁迫反应：XXM 2.0 诱导的 Ca²⁺ 信号刺激活性氧的产生和防御机制;ACR1 2.0 介导的阴离子外排触发了干旱胁迫反应。我们的研究结果表明，离散的 Ca²⁺ 信号和阴离子外排是特定代谢和转录重编程的触发因素，使植物能够适应特定的胁迫情况。我们的光遗传学方法揭示了在植物叶片内，不同的生理反应是由特定的离子通量触发的，这些离子通量伴随着类似的电信号。