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RESEARCH PRODUCT

Stomatal deregulation in Plasmopara viticola-infected grapevine leaves.

Marielle AdrianSophie TrouvelotAlain PuginLaurence MercierXavier DaireMarie-claire HéloirMathilde Allègre

subject

0106 biological sciencesStomatal conductancePLASMOPARA VITICOLAPhysiologySTOMATAL CONDUCTANCEPlant ScienceBiology01 natural sciencesPlant Epidermis03 medical and health scienceschemistry.chemical_compoundABSCISIC ACID (ABA)Guard cellBotanyVitisDOWNY MILDEWAbscisic acid030304 developmental biologyTranspirationOomycete0303 health sciencesfungifood and beveragesWaterbiology.organism_classification[SDV.BV.PEP]Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacySporePlant LeaveschemistryOomycetesGRAPEVINE (VITIS VINIFERA)Plasmopara viticolaGUARD CELLSDowny mildew010606 plant biology & botanyAbscisic Acid

description

International audience; In grapevine, the penetration and sporulation of Plasmopara viticola occur via stomata, suggesting functional relationships between guard cells and the pathogen. This assumption was supported by our first observation that grapevine (Vitis vinifera cv. Marselan) cuttings infected by P. viticola wilted more rapidly than healthy ones when submitted to water starvation. • Here, complementary approaches measuring stomatal conductance and infrared thermographic and microscopic observations were used to investigate stomatal opening/closure in response to infection. • In infected leaves, stomata remained open in darkness and during water stress, leading to increased transpiration. This deregulation was restricted to the colonized area, was not systemic and occurred before the appearance of symptoms. Cytological observations indicated that stomatal lock-open was not related to mechanical forces resulting from the presence of the pathogen in the substomatal cavity. In contrast to healthy leaves, stomatal closure in excised infected leaves could not be induced by a water deficit or abscisic acid (ABA)treatment. However, ABA induced stomatal closure in epidermal peels from infected leaves, indicating that guard cells remained functional. • These data indicate that the oomycete deregulates guard cell functioning, causing significant water losses. This effect could be attributed to a nonsystemic compound, produced by the oomycete or by the infected plant, which inhibits stomatal closure or induces stomatal opening; or a reduction of the back-pressure exerted by surrounding epidermal cells. Both hypotheses are under investigation.

10.1111/j.1469-8137.2006.01959.xhttps://pubmed.ncbi.nlm.nih.gov/17286831