|MAMIDI, SUJAN - North Dakota State University|
|Miklas, Phillip - Phil|
|TRAPP, JENNIFER - Washington State University|
|FELICETTI, ERIN - Washington State University|
|GRIMWOOD, JANE - Hudson Control Group|
|SCHMUTZ, JEREMY - Hudson Control Group|
|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: 2/22/2016
Publication Date: 7/1/2016
Citation: Mamidi, S., Miklas, P.N., Trapp, J., Felicetti, E., Grimwood, J., Schmutz, J., Lee, R., Mcclean, P. 2016. Sequence-based introgression mapping identifies candidate white mold tolerance genes in common bean. The Plant Genome. 9:1-11. doi: 10.3835/plantgenome2015.09.0092.
Interpretive Summary: Sclerotinia white mold, is an important fungal disease limiting dry bean production in the United States. It is the major constraint influencing bean production in Michigan, Minnesota, Nebraska, and North Dakota where more than 80% of the dry bean acreage is located. Tens of millions of dollars in lost farm revenue results from this disease on an annual basis. Varieties with partial genetic resistance are a critical component of integrated strategies used to control white mold in bean. This work reports on the fine mapping of genes influencing partial resistance. Two genes WM7.1 and WM8.3 (referred to as QTL -quantitative trait loci), conditioning partial resistance, were chosen because of their consistent and major effect. These two genes were integrated into a pinto bean background and genetic stocks or populations were developed to study them in more detail. Fine structure QTL mapping defined the physical location within the chromosome where the genes reside. These physical locations provided improved markers for indirect selection of the genes that will facilitate development of cultivars with partial resistance to white mold disease. Furthermore, the candidate genes identified provide scientists a basis from which to gain a better understanding of the resistance response to white mold at the physiological and molecular level.
Technical Abstract: White mold disease, caused by the necrotrophic fungus Sclerotinia sclerotiorum (Lib.) de Bary, is a major pathogen of common bean (Phaseolus vulgaris L.). More than 20 QTL were reported using multiple bi-parental populations. To study the disease in more detail, advanced back-cross populations segregating individually for two major QTL, WM7.1 and WM8.3, and a recombinant population segregating for both QTL were developed. Fine structure QTL mapping, using segregating indel markers that targeted the two QTL regions, defined the physical interval for each QTL in each population. Susceptible and tolerant DNA pools developed from the population segregating for both QTL were sequenced to a depth of 12-19x. By comparing SNP frequency differences between susceptible and tolerant pools, WM7.1 was located to a narrow region on the proximal end of chromosome Pv07. That result in combination with the physical position of flanking markers, located the QTL to a 660 kb region that contained 41 gene models. Using a similar approach, the WM8.3 introgression covered nearly the entire length of chromosome Pv08, but was narrowed to a 1.36 Mb region containing 69 gene models. The most polymorphic candidate gene in the WM7.1 region encodes a BEACH-domain protein associated with apoptosis. Within the WM8.3 region, a receptor-like protein with the potential to recognize pathogen effectors was the polymorphic gene. These candidate genes provide the starting point to further parse out the interaction effects among two key QTL conditioning white mold tolerance.