Resistance to Soybean Cyst Nematode: Rhg1

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

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

Background: 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. Results: 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. Conclusions: 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

DOES HUMAN CAPITAL MATTER FOR FDI\u27S EFFECT ON POVERTY IN LDCs?

Very few empirical studies have attempted to study the impact of foreign direct investment and its interaction with human capital on poverty alleviation in developing countries. This paper attempts to fill this gap and contribute to the literature on FDI, human capital and poverty by not only disentangling the effects of FDI on poverty but also examining this effect in the presence of human capital