ABSTRACT Stomatal development is tightly connected with the overall plant growth, while changes in environmental conditions, like elevated temperature, affect negatively stomatal formation. Stomatal ontogenesis follows a well-defined series of cell developmental transitions in the cotyledon and leaf epidermis that finally lead to the production of mature stomata. YODA signaling cascade regulates stomatal development mainly through the phosphorylation and inactivation of SPEECHLESS (SPCH) transcription factor, while HSP90 chaperones have a central role in the regulation of YODA cascade. Here, we report that acute heat stress affects negatively stomatal differentiation, leads to high phosphorylation levels of MPK3 and MPK6, and alters the expression of SPCH and MUTE transcription factors. Genetic depletion of HSP90 leads to decreased stomatal differentiation rates. Thus, HSP90 chaperones safeguard the completion of distinct stomatal differentiation steps depending on these two transcription factors under normal and heat stress conditions.

中文翻译：

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HSP90分子伴侣在正常和热应激条件下调节气孔分化

摘要 气孔发育与植物的整体生长密切相关，而环境条件的变化，如温度升高，会对气孔形成产生负面影响。气孔个体发生遵循子叶和叶表皮中一系列明确定义的细胞发育转变，最终导致成熟气孔的产生。YODA 信号级联主要通过 SPEECHLESS (SPCH) 转录因子的磷酸化和失活来调节气孔发育，而 HSP90 分子伴侣在 YODA 级联的调节中起核心作用。在这里，我们报告急性热应激对气孔分化产生负面影响，导致 MPK3 和 MPK6 的高磷酸化水平，并改变 SPCH 和 MUTE 转录因子的表达。HSP90 的遗传耗竭导致气孔分化率降低。因此，在正常和热应激条件下，取决于这两种转录因子，HSP90 分子伴侣保护不同气孔分化步骤的完成。