Progress in understanding molecular mechanisms and evolution of resistance to succinate dehydrogenase inhibiting (SDHI) fungicides in phytopathogenic fungi

被引:429
作者
Avenot, Herve F. [1 ]
Michailides, Themis J. [1 ]
机构
[1] Univ Calif Davis, Dept Plant Pathol, Kearney Agr Ctr, Kearney Agr Ctr, Parlier, CA 93648 USA
关键词
Fungal pathogens; Carboxamides; Fungicide resistance; Mutation; Complex II; Predicted fitness; BASE-LINE SENSITIVITY; COMPLEX-II SUCCINATE; UBIQUINONE OXIDOREDUCTASE; CARBOXIN RESISTANCE; BOTRYTIS-CINEREA; ALTERNARIA-ALTERNATA; BINDING SITE; BOSCALID FUNGICIDE; USTILAGO-MAYDIS; PYRACLOSTROBIN;
D O I
10.1016/j.cropro.2010.02.019
中图分类号
S3 [农学(农艺学)];
学科分类号
0901 ;
摘要
Succinate dehydrogenase (Complex II or succinate-ubiquinone oxidoreductase) is the smallest complex in the respiratory chain and transfers the electrons derived from succinate directly to the ubiquinone pool. Succinate dehydrogenase inhibitor (SDHI) fungicides specifically inhibit fungal respiration by blocking the ubiquinone-binding sites in the mitochondrial complex II and play an important role in the integrated management programmes of many plant diseases. In contrast to first generation of SDHI fungicides (e.g. carboxin) exceptionally active against basidiomycetes, newer active ingredients in this class (e.g. boscalid, penthiopyrad, fluopyram) show a broad-spectrum activity against various fungal species. However, the consistent use of site-specific fungicides such as SDHIs can result in the selection of resistant fungal genotypes which may ultimately lead to a rapid decline of fungicide performance. This paper reviews previous and recent advances in understanding the molecular mechanisms and other factors controlling the evolution of resistance to SDHI fungicides. Furthermore, we provide recommendations on the future use of new developed molecules of this group as well as future research prospects. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:643 / 651
页数:9
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