Pathogate: Stomatal control of pathogenic microbe infestation

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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.