Using GWAS to disentangle resistance and susceptibility to major soybean seedling disease pathogens

Authors: DETRANALTES, CHRISTOPHER - Purdue University; MA, JIANXIN - Purdue University; Cai, Guohong

Submitted to: American Phytopathological Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 4/15/2023
Publication Date: 8/12/2023
Citation: Detranaltes, C., Ma, J., Cai, G. 2023. Using GWAS to disentangle resistance and susceptibility to major soybean seedling disease pathogens. American Phytopathological Society Abstracts. ABSTRACT.

Interpretive Summary: N/A

Technical Abstract: Soybean seedling disease pathogens are the second worst cause of disease-related yield losses across the United States only behind soybean cyst nematode. Resistance to these major threats is poorly understood, leaving growers to gamble on planting weather or costly seed treatments to manage their losses. Discovering and understanding genes responsible for resistance and susceptibility to the predominant pathogens in the seedling disease complex is an important step towards managing these losses. Over 200 landraces and commercial varieties from the USDA germplasm collection were screened against predominant seedling pathogens including Fusarium graminearum, Pythium irregulare, P. ultimum var. sporangiiferum, and P. ultimum var. ultimum. Measures of emergence and adjusted root weight showed continuous distributions after inoculation with F. graminearum or P. irregulare across all varieties indicating a polygenic resistance and susceptibility mechanism. No varieties were found with significant resistance to either variety of P. ultimum. GWAS performed on the Fusarium and P. irregulare data uncovered significant marker trait associations (MTAs) with both resistance and susceptibility effects. Five significant MTAs each explaining 3-4% of the variation observed in both emergence and root weight were found after inoculation with Fusarium graminearum. Comparison to the published Williams82 reference genome show a susceptibility marker found on chromosome 6 lies in the middle of a GDSL-like lipase/acylhydrolase protein while another on chromosome 3 is roughly 5 kbp from an Armadillo-repeat kinesin. Two additional susceptibility MTAs on chromosome 7 and chromosome 13 are not within currently annotated regions of the genome. A minor resistance marker is located 741 bp away from an WSD1-like O-acyltransferase family protein. Two MTAs explaining ~10% each of the variation in response to P. irregulare were also found. The marker on chromosome 10 is in a polygalacturanase-like gene in a region also predicted to encode cupin, germin, and polyketide synthesis enzymes. The susceptibility marker on chromosome 15 is not located within any currently annotated regions but within 100 kbp of a leucine-rich repeat protein kinase.