Barley Rom1 reveals a potential link between race-specific and nonhost resistance responses to powdery mildew fungi

被引:14
作者
Freialdenhoven, A
Orme, J
Lahaye, T
Schulze-Lefert, P
机构
[1] Max Planck Inst Zuchtungsforsch, D-50829 Cologne, Germany
[2] John Innes Ctr Plant Sci Res, Sainsbury Lab, Norwich NR4 7UH, Norfolk, England
[3] Univ Halle Wittenberg, Inst Genet, D-69120 Halle An Der Saale, Germany
关键词
negative regulator; pathogen resistance; suppressor screen;
D O I
10.1094/MPMI-18-0291
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The Rar1 gene, identified in the context of race-specific powdery mildew resistance mediated by the Hordeum vulgare (barley) resistance (R) gene Mla12, is required for the function of many R-mediated defense responses in mono-and dicotyledonous plant species. Mla resistance is associated with an oxidative burst and a subsequent cell death reaction of attacked cells. Rar1 mutants are impaired in these responses and, to identify genetic elements which negatively regulate the Mla12-triggered response, we have screened mutagenized Mla12 rar1 mutant populations for restoration of the resistance response. Here we describe the restoration of Mla12-specified resistance (rom1) mutant that restores features of disease resistance to a Blumeria graminis f. sp. hordei isolate expressing the avirulence gene AvrMla12 and retains susceptibility to an isolate lacking AvrMla12. Histochemical analyses show that, in rom1 mutant plants, a whole-cell oxidative burst and cell death response in attacked epidermal cells is restored in the incompatible interaction. Defense responses against tested inappropriate powdery mildews, B. graminis f. sp. tritici and Golovinomyces orontii, were diminished in rar1 mutant plants and enhanced in rom1 mutant plants relative to the wild type. These findings indicate antagonistic activities of Rar1 and Rom1 and reveal their contribution to nonhost and race-specific resistance responses.
引用
收藏
页码:291 / 299
页数:9
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