Pathogate: Stomatal control of pathogenic microbe infestation

叶表面的气孔对CO2的吸收是必不可少的。然而，这些开放的缝隙也允许蒸腾作用，并为病原微生物创造了进入场所。在干旱和病原体侵袭期间，气孔关闭，从而防止水分的过度损失，并阻止任何进一步的微生物感染。气孔关闭是由保卫细胞的体积变化引起的；这种反应类似于非生物和生物胁迫信号。这个项目的目标是解开被保卫细胞识别的微生物相关分子模式的感知模块。这种生物刺激的信号机制将与干旱应激激素ABA的感知机制进行比较。尽管感知这种生物刺激的第一步与ABA不同，但信号通路在蛋白激酶开放口腔1(OST1)处汇聚。一旦被激活，OST1可以通过直接相互作用或通过额外的蛋白激酶刺激SLAC1/SLAH3质膜阴离子通道。保卫细胞中两个阴离子通道的激活对气孔关闭是最重要的。我们的目标是阐明病原体识别和OST1激活之间的连锁反应，以及随后导致气孔关闭的步骤。这些研究旨在确定气孔关闭所必需的关键成分，以及保卫细胞对病原微生物的反应所特有的成分。

Stomatal pores in the leaf surface are essential for CO2 uptake. However, these open gaps also allow transpiration and create entry sites for pathogenic microorganisms. During drought and pathogen attack, the stomata close, thereby preventing excessive loss of water and hindering any further infestation by microbes. Stomatal closure is provoked by volume changes in guard cells; a response that is similar to both abiotic and biotic stress signals. The goal of this project is to unravel the perception module for a microbe-associated molecular pattern that is recognized by guard cells. The signalling mechanisms for this biotic stimulus will be compared to the well-studied perception mechanism of the drought stress hormone ABA. Although the first steps in the perception of this biotic stimulus differ from those of ABA, the signalling pathways converge at the protein kinase Open Stomata1 (OST1). Once activated, OST1 can stimulate the SLAC1/SLAH3 plasma membrane anion channels, either by a direct interaction or via additional protein kinases. The activation of both anion channels in guard cells is of prime importance for stomatal closure. We aim to clarify the chain of events between pathogen recognition and OST1 activation, as well as the steps that follow, which culminate in stomatal closure. These studies are intended to pinpoint the key components necessary for stomatal closure, as well as elements that are specific for the guard cell response to pathogenic microorganisms.