Linked candidate genes of different functions for white mold resistance in common bean (Phaseolus vulgaris. L) are identified by QTL-based pooled sequencing

Abstract

Background White mold (WM) is a major disease in common bean ( Phaseolus vulgaris L.), and its complex quantitative genetic control has limited the development of WM resistant cultivars. WM2.2 is one of the nine meta-QTL that has a major effect on WM tolerance. This QTL explains up to 35% of the phenotypic variation and was previously mapped to a large interval on Pv02. Our objective was to narrow the interval of this QTL using QTL-based bulk segregant analysis.Results The phenotypic and genotypic data from two RIL populations (R31 and Z0726-9), which possess different genetic backgrounds for white mold resistance, were used to select resistant and susceptible lines to generate subpopulations for bulk DNA sequencing, and reads were aligned against the sequence of the resistance parent. The QTL physical intervals for each RIL population were mapped by fixed SNPs in 10kb-2kb sliding windows. WM2.2 QTL was split into two regions WM2.2a (3.54-4.56 Mbp; euchromatic) and WM 2.2b (12.19 to 26.41 Mbp; heterochromatic) in populations R31 and Z0726-9, respectively. For each QTL interval, the possible functional contribution of significant non-synonymous and synonymous polymorphisms was investigated. Gene models encoding for pentatricopeptide repeat, gibberellin 2-oxidase, and heat-shock proteins are the likely candidate genes associated with WM2.2a resistance. A TIR-NBS-LRR class of disease resistance protein and a EF-TU receptor are potential candidate genes associated with WM2.2b resistance and most likely trigger a physiological resistance response to WM.Conclusion QTL-based pooled sequencing analysis revealed that the large genomic region associated with WM2.2 meta QTL consists of two major QTL each associated with a different WM resistance function. WM2.2a region is most likely associated with avoidance mechanisms while WM2.2b region triggers physiological resistance.

Mitigating against Sclerotinia Diseases in Legume Crops: A Comprehensive Review

“…Recent studies have identified resistant genes GmGST of glutathione transferase and GmCH1 of chitinase via cloning, which increase resistance to S. sclerotiorum in soybean [155,156]. Similarly, the silencing of the endo-polygalacturonase gene (SsPG1), cellobiohydrolase gene (SsCBH), and oxaloacetate acetylhydrolase gene (SsOAH1) in B. napus led to a reduction in disease by 40%, showing the path in managing the disease via host-induced gene silencing [157]. In common bean, genomic regions WM2.2a and WM2.2b are linked to playing a role in resistance, of which the latter triggers physiological resistance and the former with avoidance mechanisms [158].…”