QTL-seq and QTL mapping identify a new locus for Cercospora leaf spot (Cercospora canescens) resistance in mungbean (Vigna radiata) and a cluster of Receptor-like protein 12 (RLP12) genes as candidate genes for the resistance.

Abstract

Key message: QTL-seq, linkage mapping, and whole-genome resequencing revealed a new locus (qCLS5.1) controlling Cercospora canescens resistance in mungbean and Receptor-like protein 12 (RLP12) genes as candidate genes for the resistance. Cercospora leaf spot (CLS) disease, caused by Cercospora canescens, is a common disease of mungbean (Vigna radiata). In this study, the genetics of CLS resistance was investigated in a new source of resistance (accession V2817) and the resistance was finely mapped to identify candidate genes. F₂ and F_2:3 populations of the cross V1197 (susceptible) × V2718 and a BC₁F₁ population of the cross V1197 × (V1197 × V2817) were used in this study. Segregation analysis suggested that the resistance is controlled by a single dominant gene. QTL-seq using F₂ individuals revealed that a single QTL (designated qCLS5.1) on chromosome 5 controlled the resistance. The qCLS5.1 was confirmed in the F_2:3 and BC₁F₁ populations by QTL analysis. Fine mapping using 978 F₂ individuals localized qCLS5.1 to a 48.94 Kb region containing three tandemly duplicated Receptor-like protein 12 (RLP12) genes. Whole-genome resequencing and alignment of V1197 and V2817 revealed polymorphisms causing amino acid changes and premature stop codons in the three RLP12 genes. Collectively, these results show that qCLS5.1 is a new locus for CLS resistance in mungbean, and a cluster of RLP12 genes are candidate genes for the resistance. The new locus qCLS5.1 will be useful for molecular breeding of durable CLS-resistant mungbean cultivars.