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Published in Journal of Plant Genome Sciences, Vol. 1 No.2 (2012) at doi: 10.5147/jpgs.2012.0055

Abstract

The genes underlying rhg1 lie at a sometimes dominant sometimes co-dominant locus, necessary for resistance to all Hg types of the soybean (Glycine max (L.) Merr.) cyst nematode (Heterodera glycines). Genomic research identified; nucleotide changes within a candidate gene encoding a receptor like kinase (RLK) that were capable of altering root development and thereby part of the resistance to Hg types 0 (race 3); changes in a laccase that are capable of altering cyst development; and genes underlying changes in membrane biology. This set of three genes are subject to co-selection with a modifier locus on another linkage block. Root development is slowed in the resistant seedling and results in end of season yield loss when SCN is not present. However, in the presence of SCN resistant seedling roots grow just as vigorously as the now slower growing parasitized susceptible roots and therefore show little loss to SCN parasitism. In some genotypes but not others the RLK can act alone to confer resistance. Functional paralogs of the three gene cluster have been found on other linkage groups including A1, B1, G, and O and these can be functional in different sources of resistance like G. soja, PI 437654 and PI438489B. At rhg1 the allele differences change the structure, interacting partners and activity of the LRR protein and the laccase. The changes between the alleles result in about 30 other proteins (judged by 2 D gels), 112 metabolites (by FTICRMS) and 8 metabolites (by GCMS) to increase in abundance in roots during SCN infection in the resistant NILs. Understanding the basis of root stunting by resistance alleles will be used to improve methods for developing new nematode resistant soybean cultivars that do not suffer from the yield suppression and low seed germination rates of existing cultivars.

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