2011 Annual Report
1a.Objectives (from AD-416)
This research is being conducted to increase the level of resistance to Sclerotinia sclerotiorum in soybean cultivars and to develop and evaluate improved disease control and resistance options for soybean producers.
1b.Approach (from AD-416)
This plan of work makes use of DNA markers and marker-assisted selection to identify and manipulate chromosomal regions that are associated with smaller lesions size when soybeans are infected with S. sclerotiorum. We are combining multiple QTL identified by the DNA marker genotypes into individual homozygous F5-serived soybean lines to increase overall resistance to the fungus. We also are evaluating different transgenic approaches that may either confer resistance to the fungus (via a lytic peptide expressed in the transgenic plants that destroys the fungus) or may allow the use of effective chemical control measures against Sclerotinia as well as other fungal and bacterial pathogens and soybean cyst nematode.
This project was initiated on June 1, 2008, research is ongoing, and the overall objective is to increase the level of resistance to Sclerotinia sclerotiorum in soybean cultivars and to develop and evaluate improved disease control and resistance options for soybean producers. ADODR monitoring activities to evaluate research progress included phone calls, meetings with the cooperator, and an annual meeting held each year in January.
Management strategies for Sclerotinia stem rot or white mold of soybean have limitations. Crop culture modifications often compromise high yield, fungicides add to production costs, and resistance found to date is partial, multigenic, and complex. This project brings together expertise and results from identification of genes involved in resistance to Sclerotinia sclerotiorumin soybean and basic research on plant defense mechanisms in response to fungal pathogen infection.Recently in Arabidopsis, LysM-containing receptor-like kinases were genetically defined as receptors for chitin. Chitin is a major component of fungal cell walls and is an established pathogen-associated molecular pattern (PAMP). This information suggests that the LysM genes represent promising candidate genes that could explain some of the resistance to white mold in selected genotypes. Analyses of soybean sequence databases indicated that soybean has 13 unique LysM-RLKs and at least another 17 LysM-domain containing proteins. The genes were cloned and sequenced. The objectives of this study are to (1) map LysM-domain encoding genes in soybean and correlate their map locations to known white mold QTL, and (2) develop SNP markers for those LysM-domain genes mapping close to known white mold QTL. Five soybean RIL populations used previously to identify QTL for sclerotinia resistance were used in this analysis. The common susceptible parent is the cultivar Williams 82. We identified 37 LysM-domain genes that were located on Linkage Groups that contained significant QTL from our previous work. We have determined that at least six of the LysM genes map to locations where we identified QTL on LGs D1b, E, F, G, K, and L. LysM genes on LG A1 and B1 were not associated with our identified QTL. For the Dassel population, the LysMe11 gene is associated with an identified QTL on LG I. The LysMe11 locus was significant in the QTL analysis, and the allele associated with smaller lesion size comes from Dassel, the resistant parent. The SNP markers that are developed in the LysM sequences could be used for marker-assisted breeding to develop near-isogenic lines with different combinations of LysM alleles for further study, and potentially cultivars with improved resistance.