The BOTRYTIS SUSCEPTIBLE1 gene encodes an R2R3MYB transcription factor protein that is required for biotic and abiotic stress responses in Arabidopsis

被引:427
作者
Mengiste, T [1 ]
Chen, X
Salmeron, J
Dietrich, R
机构
[1] Purdue Univ, Dept Bot & Plant Pathol, W Lafayette, IN 47907 USA
[2] Syngenta Biotechnol, Res Triangle Pk, NC 27709 USA
关键词
SYSTEMIC ACQUIRED-RESISTANCE; HYPERSENSITIVE CELL-DEATH; BOTRYTIS-CINEREA; SALICYLIC-ACID; NECROTROPHIC PATHOGEN; DISEASE RESISTANCE; DEFENSE RESPONSES; HYDROGEN-PEROXIDE; OXIDATIVE STRESS; OSMOTIC-STRESS;
D O I
10.1105/tpc.014167
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 molecular and cellular mechanisms involved in plant resistance to the necrotrophic fungal pathogen Botrytis cinerea and their genetic control are poorly understood. Botrytis causes severe disease in a wide range of plant species, both in the field and in postharvest situations, resulting in significant economic losses. We have isolated the BOS1 (BOTRYTIS-SUSCEPTIBLE1) gene of Arabidopsis based on a T-DNA insertion allele that resulted in increased susceptibility to Botrytis infection. The BOS1 gene is required to restrict the spread of another necrotrophic pathogen, Alternaria brassicicola, suggesting a common host response strategy against these pathogens. In the case of the biotrophic pathogens Pseudomonas syringae pv tomato and the oomycete parasite Peronospora parasitica, bos1 exhibits enhanced disease symptoms, but pathogen growth is similar in bos1 and wild-type plants. Strikingly, bos1 plants have impaired tolerance to water deficit, increased salinity, and oxidative stress. Botrytis infection induces the expression of the BOS1 gene. This increased expression is severely impaired in the coil mutant, suggesting an interaction of BOS1 with the jasmonate signaling pathway. BOS1 encodes an R2R3MYB transcription factor protein, and our results suggest that it mediates responses to signals, possibly mediated by reactive oxygen intermediates from both biotic and abiotic stress agents.
引用
收藏
页码:2551 / 2565
页数:15
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