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Pathogate: Stomatal control of pathogenic microbe infestation

Pathogate：病原微生物侵染的气孔控制

基本信息

批准号：
262167000
负责人：
Dr. Peter Ache
金额：
--
依托单位：
Lehrstuhl für Botanik I: Molekulare Pflanzenphysiologie und Biophysik
依托单位国家：
德国
项目类别：
Research Grants
财政年份：
2014
资助国家：
德国
起止时间：
2013-12-31 至 2020-12-31
项目状态：
已结题

来源：
https://gepris.dfg.de/gepris/projekt/262167000?language=en
关键词：
Pathogate Stomatal control pathogenic microbe

项目摘要

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.

叶片表面气孔对CO2的吸收至关重要。然而，这些开放的间隙也允许蒸腾作用并为病原微生物创造进入点。在干旱和病原体侵袭期间，气孔关闭，从而防止水分过度流失，阻止微生物进一步侵袭。气孔关闭是由保卫细胞的体积变化引起的；一种类似于非生物和生物应激信号的反应。这个项目的目标是解开感知模块的微生物相关的分子模式，是由保护细胞识别。这种生物刺激的信号机制将与干旱胁迫激素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，但信号通路集中在蛋白激酶OST1上。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sla1 /SLAH3质膜阴离子通道。保护细胞中两个阴离子通道的激活对气孔关闭至关重要。我们的目标是澄清病原体识别和OST1激活之间的事件链，以及随后的步骤，最终导致气孔关闭。这些研究旨在确定气孔关闭所需的关键成分，以及保护细胞对病原微生物反应的特定元素。