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ARS Home » Pacific West Area » Pullman, Washington » Grain Legume Genetics Physiology Research » Research » Publications at this Location » Publication #376627

Research Project: Developing Abiotic and Biotic Stress-Resilient Edible Legume Production Systems through Directed GxExM Research

Location: Grain Legume Genetics Physiology Research

Title: Analysis and identification of QTL for resistance to Sclerotinia sclerotiorum in pea (Pisum sativum L.)

item ASHTARI MAHINI, R - North Dakota State University
item KUMAR, AJAY - North Dakota State University
item ELIAS, ELIAS - North Dakota State University
item Fiedler, Jason
item Porter, Lyndon
item McPhee, Kevin

Submitted to: Frontiers in Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/23/2022
Publication Date: 11/19/2020
Citation: Ashtari Mahini, R., Kumar, A., Elias, E.M., Fiedler, J.D., Porter, L.D., McPhee, K.E. 2020. Analysis and identification of QTL for resistance to Sclerotinia sclerotiorum in pea (Pisum sativum L.). Frontiers in Genetics. 11. Article 587968.

Interpretive Summary: White mold is a major fungal disease on pea caused by the pathogen Sclerotinia sclerotiorum. Annual losses due to white mold in pulse crops was estimated to be as high as $12 million in the United States and significant losses are also an issue worldwide. The most economical and environment-friendly option for management of white mold is to develop disease resistant field pea varieties. Two pea lines with the best known resistance to white mold were crossed with susceptible commercial field pea cultivars to develop populations for identifying genes associated with resistance based on how the pea lines restricted the advancement of white mold. Twenty-two pea lines were identified with excellent partial resistance to white mold. Two of these lines also had short internodes and were semi-leafless, both characteristics known to help reduce white mold spread and development, respectively. Thirteen genetic regions on pea chromosomes were identified that contributed to resistance to white mold. These regions are being used to identify resistance genes and develop genetic markers that can be used to rapidly identify resistant pea lines. Identification and development of white mold resistant cultivars will dramatically reduce risks for pea growers in the US and elsewhere.

Technical Abstract: White mold caused by Sclerotinia sclerotiorum is an important constraint to field pea (Pisum sativum L.) production worldwide. To transfer white mold resistance into an adapted background, and study the genetics of the disease, two recombinant inbred line (RIL) populations (PRIL17 and PRIL19) were developed by crossing two partially resistant plant introductions with two susceptible pea cultivars. Two mapping populations, PRIL17 (Lifter × PI240515), and PRIL19 (PI169603 × Medora) were evaluated for resistance to white mold by measuring lesion expansion inhibition (LEI) and nodal transmission inhibition (NTI) at 3, 7, and 14 days post inoculation (dpi) under controlled environmental conditions. Lesion expansion inhibition percentage (LEIP), survival rate (SR) and area under disease progress curves (AUDPC) were also calculated accordingly. Because of a positive correlation between LEI and NTI with height, short and long internode individuals of each population were analyzed separately to avoid any confounding effect of height to pathogen response. A total of 22 short genotypes demonstrated partial resistance based on at least two resistance criteria. Only two pea genotypes with partial resistance to white mold (PRIL19-18 and PRIL19-124) had both semi-leafless (afila) and short internode traits. Both the RIL populations were genotyped using genotyping by sequencing (GBS). For PRIL17, a genetic map was constructed from a total of 1967 single nucleotide polymorphism (SNP) and spanned over 1494 cM representing seven linkage groups. For the PRIL19 population, a total of 1196 SNP markers were mapped to nine linkage groups with a total map distance of 1415 cM. A consensus map constructed using data from both populations, had 1486 unique SNPs over 2461 cM belonging to seven linkage groups. Inclusive composite interval mapping (ICIM) identified thirteen quantitative trait loci (QTL) associated with white mold resistance traits in both populations. Three of them were co-located with height genes (disease avoidance) and the other ten QTL were associated with two forms of resistance (seven for LEI and three for NTI). These resistance QTL might regulate defense mechanism pathway genes. The development of resistance lines, genetic dissection and identification of markers associated will help accelerate breeding efforts for white mold resistance using molecular breeding approaches.