Plants have evolved various mechanisms to defend themselves against pathogens. Many pathogens induce the formation of water-soaked lesions during early infection under conditions of high atmospheric humidity. These water-soaked spots are caused by the disruption of the plasma membrane or cell wall integrity due to various activities of effector proteins during infection. We hypothesized that bacterial PAMP-flagellin plays a role in modulating the cell-membrane permeability that controls the availability of water in the apoplast, to prevent bacterial establishment on the cell wall during the early stages of the PAMP-triggered immunity (PTI) response. Our results revealed that the conductivity of hydraulic pathways in the leaf was reduced in response to flagellin22 (flg22). The cellular osmotic water permeability (Pf) of both mesophyll cells and bundlesheath cells was dramatically reduced in response to flg22 treatment. Moreover, the whole-leaf hydraulic conductance (Kleaf) was also reduced in response to flg22 treatment. The fact that the Pf of mesophyll cells of an aquaporin (AQP) mutant was not affected by the flg22 treatment suggests the involvement of AQP channels in the flg22-induced Pf reduction signal transduction pathway. We conclude that the binding of flagellin to their receptors elicits signals to close AQPs, consequently reducing the water content of the cell wall and intercellular spaces and leading to a more negative water potential. This serves as an early PTI response to pathogen attack, which, in turn, might decrease the rate of bacterial growth and establishment in the apoplast. Significance statementWe report that the membrane osmotic water permeability of both leaf mesophyll and vascular bundle-sheath cells is reduced in response to treatment with flagellin22. We suggest that this mechanism for cell dehydration may serve as an apoplastic defense response, to limit the chances of bacterial pathogens becoming established on the walls of leaf mesophyll cells.
|Published - 2 Jan 2021
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