In this study, the antibacterial activity and mechanism of action of chlorogenic acid against bacteria were assessed. The data from minimum inhibitory concentration (MIC) values showed that chlorogenic acid effectively inhibited the growth of all tested bacterial pathogens, and the MIC values were ranging from 20 to 80 μg/mL. An investigation into action mode of chlorogenic acid against the pathogen indicated that chlorogenic acid significantly increased the outer and plasma membrane permeability, resulting in the loss of the barrier function, even inducing slight leakage of nucleotide. The leakage of cytoplasmic contents was also observed by electron micrographs. These results supported our hypothesis that chlorogenic acid bound to the outer membrane, disrupted the membrane, exhausted the intracellular potential, and released cytoplasm macromolecules, which led to cell death.
The tripeptide reduced glutathione (GSH; g-glutamate [Glu]-cysteine [Cys]-glycine) is a major endogenous antioxidant in both animal and plant cells. It also functions as a neurotransmitter mediating communication among neurons in the central nervous system of animals through modulating specific ionotropic Glu receptors (GLRs) in the membrane. Little is known about such signaling roles in plant cells. Here, we report that transient rises in cytosolic calcium triggered by exogenous GSH in Arabidopsis (Arabidopsis thaliana) leaves were sensitive to GLR antagonists and abolished in loss-of-function atglr3.3 mutants. Like the GSH biosynthesis-defective mutant PHYTOALEXIN DEFICIENT2, atglr3.3 showed enhanced susceptibility to the bacterial pathogen Pseudomonas syringae pv tomato DC3000. Pathogen-induced defense marker gene expression was also decreased in atglr3.3 mutants. Twenty-seven percent of genes that were rapidly responsive to GSH treatment of seedlings were defense genes, most of which were dependent on functional AtGLR3.3, while GSH suppressed pathogen propagation through the AtGLR3.3-dependent pathway. Eight previously identified putative AtGLR3.3 ligands, GSH, oxidized glutathione, alanine, asparagine, Cys, Glu, glycine, and serine, all elicited the AtGLR3.3-dependent cytosolic calcium transients, but only GSH and Cys induced the defense response, with the Gluinduced AtGLR3.3-dependent transcription response being much less apparent than that triggered by GSH. Together, these observations suggest that AtGLR3.3 is required for several signaling effects mediated by extracellular GSH, even though these effects may not be causally related.
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