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The receptor like kinase at Rhg1-a/Rfs2 caused pleiotropic resistance to sudden death syndrome and soybean cyst nematode as a transgene by altering signaling responses

Ali Srour12, Ahmed J Afzal123, Laureen Blahut-Beatty4, Naghmeh Hemmati1, Daina H Simmonds4, Wenbin Li5, Miao Liu5, Christopher D Town6, Hemlata Sharma17, Prakash Arelli8 and David A Lightfoot1259*

Author Affiliations

1 Department of Molecular Biology, Microbiology and Biochemistry, Southern Illinois University at Carbondale, Carbondale, IL 62901, USA

2 Department of Plant Soil and Agricultural Systems, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA

3 Department of Horticulture and Crop Science, Ohio State University, 2021 Coffey Rd, Columbus, OH 43210, USA

4 Agriculture and Agri-Food Canada, Building 21, 960 Carling Ave, Ottawa, ON K1A 0C6, USA

5 Key Laboratory of Soybean Biology in the Chinese Ministry of Education, Harbin University, Harbin, China

6 JCVI, Rockville, MD, USA

7 Department of Plant Breeding & Genetics, Rajasthan College of Agriculture, MPUAT, Udaipur, India

8 USDA, Crop Genetics Research Unit, Jackson, TN, USA

9 Genomics Core Facility; Center for Excellence the Illinois Soybean Center, Southern Illinois University at Carbondale, Carbondale, IL 62901-4415, USA

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BMC Genomics 2012, 13:368  doi:10.1186/1471-2164-13-368

Published: 2 August 2012



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. This study examined the role of a receptor like kinase (RLK) GmRLK18-1 (gene model Glyma_18_02680 at 1,071 kbp on chromosome 18 of the genome sequence) within the Rhg1/Rfs2 locus in causing resistance to SCN and SDS.


A BAC (B73p06) encompassing the Rhg1/Rfs2 locus was sequenced from a resistant cultivar and compared to the sequences of two susceptible cultivars from which 800 SNPs were found. Sequence alignments inferred that the resistance allele was an introgressed region of about 59 kbp at the center of which the GmRLK18-1 was the most polymorphic gene and encoded protein. Analyses were made of plants that were either heterozygous at, or transgenic (and so hemizygous at a new location) with, the resistance allele of GmRLK18-1. Those plants infested with either H. glycines or F. virguliforme showed that the allele for resistance was dominant. In the absence of Rhg4 the GmRLK18-1 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%). In the presence of Rhg4 the plants with the transgene were nearly classed as fully resistant to SCN (females reduced to 11% of the susceptible control) as well as SDS. 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.


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. Stable resistance to many pathogens might be achieved by manipulation the genes encoding a small number of pathogen recognition proteins.

Segregation; Pleiotropy; Rhg1/Rfs2; Soybean; Resistance; Soybean cyst nematode (SCN); Sudden death syndrome (SDS); Insect herbivory