Integrating de novo QTL-seq and linkage mapping to identify quantitative trait loci conditioning physiological resistance and avoidance to white mold disease in dry bean.

Authors: ROY, JAYANTA - North Dakota State University; SOLER-GARZON, ALVARO - Washington State University; Miklas, Phillip - Phil; CLEVENGER, JOSH - Hudsonalpha Institute For Biotechnology; LEE, RIAN - North Dakota State University; MCCLEAN, PHIL - North Dakota State University

Submitted to: The Plant Genome
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/4/2023
Publication Date: 8/21/2023
Citation: Roy, J., Soler-Garzon, A., Miklas, P.N., Clevenger, J., Lee, R., Mcclean, P. 2023. Integrating de novo QTL-seq and linkage mapping to identify quantitative trait loci conditioning physiological resistance and avoidance to white mold disease in dry bean.. The Plant Genome. 16(4):e20380. https://doi.org/10.1002/tpg2.20380.
DOI: https://doi.org/10.1002/tpg2.20380

Interpretive Summary: White mold continues to be a devastating disease of dry bean. Integrated control methods are required to combat this disease. In our lab we have focused on breeding for genetic resistance to this pathogen. This work describes further characterization and validation of five genes that condition partial resistance to white mold. Narrowed genomic intervals reveal candidate genes that can be leveraged for improved markers for genomic assisted selection to facilitate breeding dry beans with improved resistance to white mold. This disease causes millions in lost revenue each year and cultivars with improved resistance will help to combat this loss.

Technical Abstract: White mold (WM), caused by the ubiquitous fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a devastating disease that limits production and quality of common bean globally. The complex host-pathogen interaction and lack of complete host resistance coupled with low to medium heritability often limits breeding efforts to develop improved WM resistant dry bean cultivars. In the present study, classic linkage mapping combined with QTL-seq were employed in two recombinant inbred line (RIL) populations, ‘Montrose’/I9365-25 (M25) and ‘Raven’/I9365-31 (R31), with the goal of fine-mapping QTL WM5.4 and WM7.5 that condition WM resistance. The RILs were phenotyped for WM reactions under greenhouse (straw test) and field environments. WM5.4 and WM7.5 were reconfirmed with both mapping strategies within each population. Combining the results from both mapping strategies, WM5.4 was delimited within 22.60-36.25 Mb interval located in the heterochromatic regions on Pv05, while WM7.5 was narrowed to a 0.83-Mb (3.99-4.82 Mb) region on the Pv07 chromosome. Furthermore, two additional QTL WM2.2a (3.81-7.24 Mb) and WM2.2b (23.33-25.94 Mb) were mapped to a narrowed genomic interval on Pv02 and WM4.2 in a 0.89 Mb physical interval at the distal end of Pv04 chromosome. Gene models encoding gibberellin 2-oxidase proteins regulating plant architecture are likely candidate genes associated with WM2.2a resistance. Nine gene models encoding a disease resistance protein (quinone reductase family protein and ATWRKY69 etc) found within the WM5.4 QTL interval are putative candidate genes. Clusters of 13 and 5 copies of gene models encoding cysteine-rich receptor-like kinase and receptor-like protein kinase-related family proteins, respectively are potential candidate genes associated with WM7.5 resistance and most likely trigger physiological resistance to WM. Acquired knowledge of the narrowed major QTL intervals, flanking markers, and candidate genes provides promising opportunities to develop functional molecular markers to implement marker-assisted selection for WM resistant dry bean cultivars.