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Plant J. 2010 Jul 1;63(1):115-27. doi: 10.1111/j.1365-313X.2010.04224.x. Epub 2010 Apr 7.

Tryptophan-derived secondary metabolites in Arabidopsis thaliana confer non-host resistance to necrotrophic Plectosphaerella cucumerina fungi.

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Centro de Biotecnología y Genómica de Plantas (UPM-INIA), Universidad Politécnica de Madrid, Campus Montegancedo, E-28223-Pozuelo de Alarcón, Madrid, Spain.


A defence pathway contributing to non-host resistance to biotrophic fungi in Arabidopsis involves the synthesis and targeted delivery of the tryptophan (trp)-derived metabolites indol glucosinolates (IGs) and camalexin at pathogen contact sites. We have examined whether these metabolites are also rate-limiting for colonization by necrotrophic fungi. Inoculation of Arabidopsis with adapted or non-adapted isolates of the ascomycete Plectosphaerella cucumerina triggers the accumulation of trp-derived metabolites. We found that their depletion in cyp79B2 cyp79B3 mutants renders Arabidopsis fully susceptible to each of three tested non-adapted P. cucumerina isolates, and super-susceptible to an adapted P. cucumerina isolate. This assigns a key role to trp-derived secondary metabolites in limiting the growth of both non-adapted and adapted necrotrophic fungi. However, 4-methoxy-indol-3-ylmethylglucosinolate, which is generated by the P450 monooxygenase CYP81F2, and hydrolyzed by PEN2 myrosinase, together with the antimicrobial camalexin play a minor role in restricting the growth of the non-adapted necrotrophs. This contrasts with a major role of these two trp-derived phytochemicals in limiting invasive growth of non-adapted biotrophic powdery mildew fungi, thereby implying the existence of other unknown trp-derived metabolites in resistance responses to non-adapted necrotrophic P. cucumerina. Impaired defence to non-adapted P. cucumerina, but not to the non-adapted biotrophic fungus Erysiphe pisi, on cyp79B2 cyp79B3 plants is largely restored in the irx1 background, which shows a constitutive accumulation of antimicrobial peptides. Our findings imply differential contributions of antimicrobials in non-host resistance to necrotrophic and biotrophic pathogens.

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