The receptor like kinase transgene at Rhg1/Rfs2 causes resistance to sudden death syndrome and soybean cyst nematode

Soybean (Glycine max L. Merr.) resistance to any population of  Heterodera glycines, the cyst nematode (SCN) or Fusarium virguliforme agent of sudden death syndrome (SDS), required a functional allele at Rhg1/Rfs2. SCN was an endemic, ancient, pest of soybean whereas F. virguliforme was a recent, regional, pest. This study examined the role of a receptor like kinase (RLK) GmRLK18-1 (gene model Gm_0121_x00208 at 1,071 kbp on chromosome 18 of the genome sequence) within the Rhg1/Rfs2 locus in resistance to SCN and SDS. Sequence alignments showed the resistance allele was an introgressed region of about 73.8 kbp. Analysis of  plants that were either heterozygous at Rhg1/Rfs2  or transgenic and so hemizygous with the resistance allele of GmRLK18-1 at a new location were made. Those plants infested with either H. glycines or F. virguliforme showed that the allele for resistance was dominant. The RLK was sufficient to confer nearly complete resistance to both root and leaf symptoms of SDS and provide partial resistance to three different populations of nematodes (mature female cysts were reduced by 30-50%). A reduction in the rate of  early seedling root development was also shown to be caused by the resistance allele of the GmRLK18-1.  Field trials of transgenic plants showed an increase in foliar susceptibility to insect herbivory. Proteomic analysis showed that GmRLK18-1 increased the abundance of proteins in the salicylic acid pathways but interfered with jasmonate signaling involved in resistance to insect herbivory. The inference that soybean has adapted part of an existing pathogen recognition and defense cascade (H.glycines; SCN and insect herbivory)  to a new pathogen (F. virguliforme; SDS) has broad implications for crop improvement.