Overexpression of AHL20 Negatively Regulates Defenses in Arabidopsis

来源 :Journal of Integrative Plant Biology | 被引量 : 0次 | 上传用户:wudi120
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Plants are equipped to recognize invading pathogenic microbes and activate innate immune responses by sensing pathogen-associated molecular patterns(PAMPs).PAMP-triggered immunity(PTI) is critical for plant resistance to potential pathogens.Although the mechanism by which PTI is activated has been intensively studied,exactly how plants prevent unregulated immune responses is less well understood.Here we provide evidence that AHL20,an AT-hook containing DNA-binding protein,negatively regulates PTI.Overexpression of AHL20 as a stable transgene suppressed PAMP-induced NHO1 and FRK1 expression in Arabidopsis plants.Similarly,transient expression of the closely related family members AHL19,AHL15,and AHL27 in protoplasts also blocked PAMP-induced gene expression.The AHL20 overexpression plants displayed greater susceptibility to virulent Pseudomonas syringae bacteria.These results indicate that AHL proteins play an important role in plant immunity. Plants are equipped to recognize invading pathogenic microbes and activate innate immune responses by sensing pathogen-associated molecular patterns (PAMPs). PAMP-triggered immunity (PTI) is critical for plant resistance to potential pathogens. Although the mechanism by which PTI is activated has been intensively studied, exactly how plants prevent unregulated immune responses is less well understood. Here we provide evidence that AHL20, an AT-hook containing DNA-binding protein, negatively regulates PTI. Overexpression of AHL20 as a stable transgene suppressed PAMP-induced NHO1 and FRK1 expression in Arabidopsis plants.Similarly, transient expression of the closely related family members AHL19, AHL15, and AHL27 in protoplasts also blocked PAMP-induced gene expression.The AHL20 overexpression plants showed greater susceptibility to virulent Pseudomonas syringae bacteria.These results indicate that AHL proteins play an important role in plant immunity.
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