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Fine mapping of QTL conferring Cercospora leaf spot disease resistance in mungbean revealed TAF5 as candidate gene for the resistance
Thursday, 2021/02/25 | 08:22:44

Chutintorn YundaengPrakit SomtaJingbin ChenXingxing YuanSompong Chankaew & Xin Chen

Theoretical and Applied Genetics February 2021; vol. 134: 701–714.

 

Figure: Symptoms of Cercospora leaf spot in mungbean

Key message

This paper reports fine 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

Abstract

Cercospora leaf spot (CLS) caused by the fungus Cercospora canescens is an important disease of mungbean. A QTL mapping using mungbean F2 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 × (KPS1 × V4718)] population developed in this study and the F2 (KPS1 × V4718) population used in a previous study were genotyped with 16 newly developed SSR markers. QTL analysis in the BC8F2 and F2 populations consistently showed that the qCLS was mapped to a genomic region of ~ 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.

 

See https://link.springer.com/article/10.1007/s00122-020-03724-8

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