Location: Sunflower and Plant Biology Research2012 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.
3. Progress Report:
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. The innate immunity responses of six soybean genotypes, which show different resistance levels to white mold, were analyzed after treatment with flagellin 22 (flg22) or chitin. As an indicator of innate immunity we measured the production of reactive oxygen species (ROS) and nitric oxide (NO), which are well established responses of innate immunity. Our analysis showed that flg22 induced a stronger ROS production than chitin treatment and also that the production of either ROS or NO was genotype dependent. Likewise, we observed that the genotype Vinton81 produced more ROS triggered by flg22 than the other five genotypes; in contrast Williams 82 produced more ROS after chitin treatment. When NO production was measured, we observed that Corsoy 79 was the genotype that produced more NO in either of the two treatments. Preliminary results of the QTL analysis to correlate specific genetic regions with the variation that we see in ROS production indicate that there are some genomic regions associated with ROS production that correlate with our previously identified QTL for response to Sclerotinia infection, or with regions where other identified resistance genes are mapped. With the addition of the 1536 SNP genotype information to our previous SSR genetic linkage map, we were able to identify some additional QTL related to lesion size in our detached leaf assay with S. sclerotiorum mycelium plugs. Preliminary analysis from our first replication of ROS data from the UX992 soybean population (Vinton 81 x Williams 82) shows correspondence of a QTL peak for Sclerotinia lesion size and for ROS production at 75-90 cm on chromosome 1. One of the most significant QTL in the UX992 population, as well as others in the initial QTL analysis by Arahana et al (2001) was the QTL on chromosome 10 (LG O). In our current analysis, there is a peak for the ROS production data that corresponds to the same genomic regions identified as lesion size QTL. Another interesting result from this preliminary analysis is the peak for ROS production around 50-70 cM on chromosome 13 that corresponds to the region where other resistance QTL and resistance genes have been mapped, including bacterial blight, phytophthora root rot, soybean mosaic virus, peanut root-knot nematode, javanese root-knot nematode, and Sclerotinia lesion size QTL from our previous study.