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Jianqiang Miao, Wenjun Mu, Yang Bi, Yanling Zhang, Shaoliang Zhang, Jizhen Song, Xili Liu.Heterokaryotic state of a point mutation (H249Y) in SDHB protein drives the evolution of thifluzamide resistance in Rhizoctonia solani

作者:  来源:DOI:10.1002/ps.6155  发布日期:2020-10-23  浏览次数:

Heterokaryotic state of a point mutation (H249Y) in SDHB protein drives the evolution of thifluzamide resistance in Rhizoctonia solani

Jianqiang Miao, Wenjun Mu, Yang Bi, Yanling Zhang, Shaoliang Zhang, Jizhen Song, Xili Liu

Pest Management Science

DOI:10.1002/ps.6155

Abstract

Background: The sheath blight, caused by Rhizoctonia solani, can be effectively controlled by the application of the succinate dehydrogenase inhibitor (SDHI) thifluzamide. Although the resistant risk of thifluzamide in R. solani had been reported, but the thifluzamide-resistance mechanism and the evolution of thifluzamide-resistance in R. solani have not been investigated in detail.

Results: No differences were found between the sequences of the SDHA, SDHC and SDHD protein among the thifluzamide-sensitive isolates and the thifluzamide-resistant mutants, but a single point mutation H249Y was found in SDHB protein. Two different types of thifluzamide-resistant R. solani mutants were characterized: homokaryotic type, carrying only the resistance allele, and heterokaryotic type, retaining the wild-type allele in addition to the resistance allele. The resistance level differed according to nuclear composition at position of codon 249 in sdhB gene. Molecular docking results suggested that the point mutation (H249Y) might significantly altered the affinity of thifluzamide and SDHB protein. Heterokaryotic mutants were able to evolve into a homokaryon when repeatedly cultured on agar media or rice plants in the presence of thifluzamide, but thifluzamide treatment had no effect on the genotypes of the homokaryotic mutants or the sensitive isolates.

Conclusion: This study showed that H249Y in SDHB protein could cause thifluzamide-resistance in R. solani. Fungicide application could promote heterokaryotic mutants to evolve into a homokaryon. This article is protected by copyright.