| In nature, phytopathogen usually initiates its infection on leaf surface before moving into the internal space through nature openings. Little is known about immediate response of the leaf to the surface-colonizing phytopathogen and its correlation with individual microbe-associated molecular patterns (MAMPs). In this study we monitored dynamic change of cytosolic Ca2+concentration [Ca2+]cyt in the Arabidopsis leaf expressing luminance protein aequorin as response to surface inoculating Pst DC3000. Significant [Ca2+]cyt transient rise was evoked in the leaf right after the inoculation and the magnitude was correlated with the pathogen concentration. Pharmacological studies revealed that the rising [Ca2+]cyt was primarily from cAMP-mediated Ca2+mobility pathway, but not Gd3+sensitive Ca2+influx channel in the plasma membrane, which was distinct from those induced by individual MAMPs (Lipopolysaccharide, flagellin and elongation factor Tu). Pretreating the leaf with Pst DC3000or the MAMPs significantly attenuated its responses to subsequent treatments of the any, which indicated that the leaf had convergent sensitivity mechanism to the pathogen and the MAMPs. Furthermore, Pst DC3000’s mutants defective in flagellum, type III secretion apparatus and phytotoxin coronine production significantly lost their multiplication ability in the leaf apoplast, but evoked the wild type comparable [Ca2+]cyt responses. Taken together, these data indicates that the [Ca2+]cyt in the leaf has sensitive response to the surface-inoculating phytopathogen, which was distinct from those of individual MAMPs and had no correlation with the pathogen’s pathogenesis capacity.Lipopolysaccharide (LPS) is a core component within cell walls of gram-negative bacterial. It triggers defense-related responses in plants. It is unknown of molecular mechanism of LPS perception by plant cells. In this study we found that LPS induced endocytosis of Arabidopsis guard cell hydrogn peroxide-resistant1(AtGHRl), a homolog of toll-like receptor4(TLR4), complex of which confers LPS sensing of animal cells. AtGHRl partially mediates LPS-evoked transient rise of reactive oxygen species, nitrate oxide and cytosolic Ca2+with desensitization feature. It also mediated about45%LPS-triggered transcriptional responses in the leaf. Leaves of Arabidopsis AtGHRl loss-of-function mutants were defective in the LPS-triggered defense response to pseudomonas syringae pv. tomato Pst DC3000. Token together, this study identified a novel key genetic component in the LPS-induced innate immunity in plants. |