Abstract
Regulation of stomatal aperture is of critical importance to plants to balance gas exchange and water loss, and also to control ingress of bacterial pathogens. MAP kinase signal transduction pathways are mediators of biotic and abiotic stress, and have been indicted in the control of stomatal movements. Cell-specific antisense was used to down-regulate MPK3 gene expression in Arabidopsis guard cells, resulting in ABA insensitivity during inhibition of stomatal opening, but a normal ABA response in promotion of closure assays. This response is similar to that of the heterotrimeric G protein alpha subunit mutant gpa1, as is the imposition of ABA insensitivity during stomatal closure by butyrate treatment, suggesting that MPK3 and GPA1 are in the same ABA signal transduction pathway and adding further evidence for parallel signalling pathways during ABA-induced closure. By contrast, antisense plants were less sensitive to H2O2 in both promotion of closure and inhibition of opening assays, although H2O2 production in response to ABA was not affected. Regulation of stomatal aperture by PAMPs has recently been shown to be an important plant defense mechanism; since MPK3 is also activated by such pathogen elicitors, we postulate that in addition to a signalling role in guard cell movements, MPK3 is involved in the active prevention of bacterial infection through stomata.
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