Hyper-Polymorphism Around Resistance Loci of Soybean

Soybean (Glycine max (L. Merr.)) resistance to any population of  Heterodera glycines (I.), or Fusarium virguliforme (Akoi, O’Donnell, Homma & Lattanzi) required a functional allele at Rhg1/Rfs2. H. glycines, the soybean cyst nematode (SCN) was an ancient, endemic, pest of soybean whereas F. virguliforme causal agent of sudden death syndrome (SDS), was a recent, regional, pest. The role of a receptor like kinase (RLK) GmRLK18-1 (Glyma_18_02680) was within the Rhg1/Rfs2 locus and causes  resistance to SCN and SDS in trans- (actually cis-) genic plants. An 82 kbp BAC (B73p06) encompassing DNA from Peking introgressed into Forrest was sequenced from a resistant cultivar and compared to the sequences of two susceptible cultivars from which exactly 800 SNPs were found. Across 62 sequenced genomes few additional SNPs were found. There were only 18 SNPs between susceptible cultivars. A similar pattern was found at Rhg4 another unlinked locus. However the BAC did not encompass the repeat region inferred to be linked to Rhg1 in other studies. The RLK as a cis-geneic was sufficient to confer nearly complete resistance to both root and leaf symptoms of SDS caused by F. virguliforme and provided partial resistance to three different populations of nematodes (mature female cysts were reduced by 30-50%). Field trials of transgenic plants from 2010-2014 showed an increase in resistance to SDS and SCN. The inference that soybean has adapted part of an existing pathogen recognition and defense cascade (H.glycines; SCN)  to a new pathogen (F. virguliforme; SDS) was supported by immunolocalization and ligand binding of the protein. Therefore, there are broad implications for crop improvement. Stable resistance to many pathogens might be achieved by manipulation the genes encoding a small number of pathogen recognition proteins.