O'Mara Sean P, Broz Karen, Schwister Erin M, Singh Lovepreet, Dong Yanhong, Elmore J Mitch, Kistler H Corby
Department of Agronomy and Plant Genetics, University of Minnesota, St. Paul, MN 55108.
U.S. Department of Agriculture-Agricultural Research Service Cereal Disease Laboratory, St. Paul, MN 55108.
Phytopathology. 2023 Oct;113(10):1916-1923. doi: 10.1094/PHYTO-09-22-0345-R. Epub 2023 Nov 14.
The plant pathogenic fungus is the causal agent of Fusarium head blight (FHB) disease on small-grain cereals. produces trichothecene mycotoxins such as deoxynivalenol (DON) that are required for full virulence. DON must be exported outside the cell to cause FHB disease, a process that may require the involvement of membrane-bound transporters. In this study, we show that the deletion of membrane-bound transporters results in reduced DON accumulation as well as reduced FHB symptoms on wheat. Deletion of the ATP-binding cassette (ABC) transporter gene results in the greatest reduction in DON accumulation and virulence. Deletion of another ABC transporter gene, , also reduces FHB symptoms to a lesser degree. Combining deletions fails to reduce DON accumulation or virulence in an additive fashion, even when a ∆ deletion is included. Heterologous expression of transporters in a DON-sensitive strain of yeast confirms Abc1 as a major DON resistance mechanism; furthermore, it suggests that Abc1 is directly participating in DON transport rather than facilitating DON transport though other means. Yeast expression further indicates that multiple transporters, including Abc1, play an important role in resistance to the wheat phytoalexin 2-benzoxazolinone (BOA) and other xenobiotics. Thus, Abc1 may contribute to virulence on wheat both by facilitating export of DON and by providing resistance to the wheat phytoalexin BOA. This research provides useful information that may aid in designing novel management techniques of FHB or other destructive plant diseases.
这种植物病原真菌是小粒谷物上镰刀菌穗腐病(FHB)的致病因子。它产生诸如脱氧雪腐镰刀菌烯醇(DON)等单端孢霉烯族毒素,这些毒素是完全致病力所必需的。DON必须输出到细胞外才能引发FHB病害,这一过程可能需要膜结合转运蛋白的参与。在本研究中,我们表明膜结合转运蛋白的缺失导致DON积累减少以及小麦上FHB症状减轻。ATP结合盒(ABC)转运蛋白基因的缺失导致DON积累和致病力的最大程度降低。另一个ABC转运蛋白基因的缺失也在较小程度上减轻了FHB症状。即使包含∆缺失,联合缺失也不能以累加方式降低DON积累或致病力。在对DON敏感的酵母菌株中异源表达转运蛋白证实Abc1是主要的DON抗性机制;此外,这表明Abc1直接参与DON转运,而不是通过其他方式促进DON转运。酵母表达进一步表明,包括Abc1在内的多种转运蛋白在对小麦植保素2 - 苯并恶唑啉酮(BOA)和其他异生物质的抗性中起重要作用。因此,Abc1可能通过促进DON的输出以及对小麦植保素BOA提供抗性来促进对小麦的致病力。这项研究提供了有用的信息,可能有助于设计FHB或其他破坏性植物病害的新型管理技术。