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Plant J. 2011 Sep;67(6):980-92. doi: 10.1111/j.1365-313X.2011.04651.x. Epub 2011 Jul 6.

Arabidopsis ENHANCED DISEASE RESISTANCE 1 is required for pathogen-induced expression of plant defensins in nonhost resistance, and acts through interference of MYC2-mediated repressor function.

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Graduate School of Agriculture, Kyoto University, Kyoto, Japan.


Arabidopsis thaliana exhibits durable resistance, called nonhost resistance, against non-adapted fungal pathogens that typically terminates pathogen entry. The PEN2-dependent indole glucosinolate metabolism pathway is involved in preventing the entry of a range of non-adapted fungi. Here, we report that ENHANCED DISEASE RESISTANCE 1 (EDR1) functions in pre-invasive nonhost resistance. Plants lacking EDR1 exhibit impaired entry resistance to the non-adapted hemibiotrophic Colletotrichum gloeosporioides, in contrast to the enhanced resistance of edr1 against biotrophic infection of a host-adapted powdery mildew fungus. Analysis of the edr1 pen2 double mutant indicates that EDR1 acts in a defense pathway independent from the PEN2 indole glucosinolate pathway. The edr1 mutant also exhibited enhanced susceptibility to host-adapted pathogens, including Colletotrichum higginsianum and necrotrophic Alternaria brassicicola. Comparative transcript profiling revealed that upon C. gloeosporioides inoculation, the expression of four plant defensin genes was severely impaired in edr1, indicating that EDR1 is required for the induced expression of these antifungal proteins. Inactivation of the MYC2-encoded transcription factor fully restored defensin expression in edr1, implying that EDR1 interferes with MYC2 function to abrogate repression of defensin expression. Furthermore, constitutive expression of plant defensin PDF1.2b largely rescued pre-invasive resistance responses in edr1 plants. These results indicate that EDR1 exerts a positive and critical role in resistance responses to hemibiotrophic/necrotrophic fungi, in part by inducing antifungal protein expression through derepression of MYC2 function.

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