Stomatal ontogenesis, patterning, and function are hallmarks of environmental plant adaptation, especially to conditions limiting plant growth, such as elevated temperatures and reduced water availability. The specification and distribution of a stomatal cell lineage and its terminal differentiation into guard cells require a master regulatory protein phosphorylation cascade involving the YODA mitogen-activated protein kinase kinase kinase. YODA signaling results in the activation of MITOGEN-ACTIVATED PROTEIN KINASEs (MPK3 and MPK6), which regulate transcription factors, including SPEECHLESS (SPCH). Here, we report that acute heat stress affects the phosphorylation and deactivation of SPCH and modulates stomatal density. By using complementary molecular, genetic, biochemical, and cell biology approaches, we provide solid evidence that HEAT SHOCK PROTEINS 90 (HSP90s) play a crucial role in transducing heat-stress response through the YODA cascade. Genetic studies revealed that YODA and HSP90.1 are epistatic, and they likely function linearly in the same developmental pathway regulating stomata formation. HSP90s interact with YODA, affect its cellular polarization, and modulate the phosphorylation of downstream targets, such as MPK6 and SPCH, under both normal and heat-stress conditions. Thus, HSP90-mediated specification and differentiation of the stomatal cell lineage couples stomatal development to environmental cues, providing an adaptive heat stress response mechanism in plants.

气孔的发生，模式和功能是环境植物适应的标志，特别是在限制植物生长的条件下，例如温度升高和水供应减少。气孔细胞谱系的规范和分布及其向分化为保卫细胞的终末分化需要涉及YODA丝裂原活化蛋白激酶激酶的主调节蛋白磷酸化级联反应。YODA信号传导导致MITOGEN激活的蛋白激酶（MPK3和MPK6）活化，这些激酶调节转录因子，包括SPEECHLESS（SPCH）。在这里，我们报告说，急性热应激会影响SPCH的磷酸化和失活并调节气孔密度。通过使用互补的分子，遗传，生化和细胞生物学方法，我们提供有力的证据表明，抗热蛋白90（HSP90s）在通过YODA级联传导热应激反应中起着至关重要的作用。遗传研究表明，YODA和HSP90.1具有上位性，它们可能在调节气孔形成的同一发育途径中线性发挥作用。HSP90与YODA相互作用，影响其细胞极化，并在正常和热应激条件下调节下游靶标（如MPK6和SPCH）的磷酸化。因此，HSP90介导的气孔细胞谱系的规范和分化将气孔发育与环境线索相结合，从而为植物提供了一种适应性的热胁迫响应机制。它们可能在调节气孔形成的同一发育途径中线性发挥作用。HSP90与YODA相互作用，影响其细胞极化，并在正常和热应激条件下调节下游靶标（例如MPK6和SPCH）的磷酸化。因此，HSP90介导的气孔细胞谱系的规范和分化将气孔发育与环境线索相结合，从而为植物提供了一种适应性的热胁迫响应机制。它们可能在调节气孔形成的同一发育途径中线性发挥作用。HSP90与YODA相互作用，影响其细胞极化，并在正常和热应激条件下调节下游靶标（例如MPK6和SPCH）的磷酸化。因此，HSP90介导的气孔细胞谱系的规范和分化将气孔发育与环境线索相结合，从而为植物提供了一种适应性的热胁迫响应机制。