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Fine mapping of QTL conferring Cercospora leaf spot disease resistance in mungbean revealed TAF5 as candidate gene for the resistance

文献类型： 外文期刊

作者： Yundaeng, Chutintorn 1 ; Somta, Prakit 2 ; Chen, Jingbin 1 ; Yuan, Xingxing 1 ; Chankaew, Sompong 4 ; Chen, Xin 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Ind Crops, Nanjing 210014, Jiangsu, Peoples R China

2.Kasetsart Univ, Fac Agr Kamphaeng Saen, Dept Agron, Kamphaeng Saen 73140, Nakhon Pathom, Thailand

3.Ctr Excellence Agr Biotechnol AG BIO PERDO CHE, Bangkok 10900, Thailand

4.Khon Kaen Univ, Dept Agron, Fac Agr, Khon Kaen 40002, Thailand

期刊名称：THEORETICAL AND APPLIED GENETICS （ 影响因子：5.699； 五年影响因子：5.565 ）

ISSN： 0040-5752

年卷期： 2021 年 134 卷 2 期

页码：

收录情况： SCI

摘要： Key message This paper reports fin mapping of qCLS for resistance to Cercospora leaf spot disease in mungbean and identified LOC106765332encoding TATA-binding-protein-associated factor 5 (TAF5) as the candidate gene for the resistance Cercospora leaf spot (CLS) caused by the fungus Cercospora canescens is an important disease of mungbean. A QTL mapping using mungbean F-2 and BC1F1 populations developed from the "V4718" (resistant) and "Kamphaeng Saen 1" (KPS1; susceptible) has identified a major QTL controlling CLS resistance (qCLS). In this study, we finely mapped the qCLS and identified candidate genes at this locus. A BC8F2 [KPS1 x (KPS1 x V4718)] population developed in this study and the F-2 (KPS1 x V4718) population used in a previous study were genotyped with 16 newly developed SSR markers. QTL analysis in the BC8F2 and F-2 populations consistently showed that the qCLS was mapped to a genomic region of similar to 13 Kb on chromosome 6, which contains only one annotated gene, LOC106765332 (designated "VrTAF5"), encoding TATA-binding-protein-associated factor 5 (TAF5), a subunit of transcription initiation factor IID and Spt-Ada-Gcn5 acetyltransferase complexes. Sequence comparison of VrTAF5 between KPS1 and V4718 revealed many single nucleotide polymorphisms (SNPs) and inserts/deletions (InDels) in which eight SNPs presented in eight different exons, and an SNP (G4,932C) residing in exon 8 causes amino acid change (S250T) in V4718. An InDel marker was developed to detect a 24-bp InDel polymorphism in VrTAF5 between KPS1 and V4718. Analysis by RT-qPCR showed that expression levels of VrTAF5 in KPS1 and V4718 were not statistically different. These results indicated that mutation in VrTAF5 causing an amino acid change in the VrTAF5 protein is responsible for CLS resistance in V4718.

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