Correlation of defense gene induction defects with powdery mildew susceptibility in
Arabidopsis
enhanced disease susceptibility mutants |
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Authors: | T Lynne Reuber Julia M Plotnikova Julia Dewdney Elizabeth E Rogers William Wood Frederick M Ausubel |
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Institution: | ;Department of Molecular Biology, Massachusetts General Hospital, and ;Department of Genetics, Harvard Medical School, Wellman 10, Massachusetts General Hospital, Boston, MA 02114, USA and ;Harvard College, Cambridge, MA, USA |
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Abstract: | We investigated the relative importance of specific Arabidopsis thaliana genes in conferring resistance to bacterial versus fungal pathogens. We first developed a pathosystem involving the infection of Arabidopsis accession Columbia with a virulent isolate of the obligate biotrophic fungal pathogen Erysiphe orontii. E. orontii elicited the accumulation of mRNAs corresponding to the defense-related genes PR1, BGL2 (PR2), PR5 and GST1 , but did not elicit production of the phytoalexin camalexin or the accumulation of defensin ( PDF1.2 ) or thionin ( THI2.1 ) mRNAs. We tested a set of 15 previously isolated Arabidopsis phytoalexin deficient (pad), non-expresser of PR (npr) and enhanced disease susceptibility (eds) mutants that are more susceptible to Pseudomonas syringae for their susceptibility to E. orontii. Four of these mutants ( pad4–1, npr1–1, eds5–1 and a double npr1–1 eds5–1 mutant) as well as Arabidopsis lines carrying a nahG transgene exhibited enhanced susceptibility to E. orontii and reduced levels of PR gene expression . Comparison of the PR gene induction patterns in response to E. orontii in the various mutants and in the nahG transgenics suggests the existence of NPR1 -independent salicylate-dependent and NPR1 -independent salicylate-independent defense gene activation pathways. Eleven other eds and pad mutants did not show measurable enhanced susceptibility to E. orontii , suggesting that these mutants are defective in factors that are not important for the limitation of E. orontii growth. |
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