Abstract

The objective of this work was to identify genomic regions that underlie resistance to Fusarium tucumaniae sp. nov., the causing agent of sudden death syndrome (SDS) in soybean in South America, using a population with a genetic background different from that previously reported for Fusarium virguliforme sp. nov. (F. solani f. sp. glycines), also responsible for SDS in soybean. Although major genes and quantitative trait loci (QTL) for SDS resistance have been identified, little is known about the same disease caused by Fusarium tucumaniae sp. nov., in South America. To identify genetic factors related to resistance to F. tucumaniae and DNA markers associated with them, a QTL analysis was performed using recombinant inbred lines. The map locations of the four loci, here identified, differed from those SDS resistance QTL previously described. It was screened a residual heterozygous line (RHL), which was heterozygous around the most effective QTL, RSDS1, and homozygous for the other genomic regions. The genetic effect of RSDS1 was confirmed using near-isogenic lines (NIL) derived from the RHL. The line which was homozygous for the Misuzudaizu genotype showed resistance levels comparable with that of the line homozygous for the Moshidou Gong 503 genotype.

Highlights

  • Resistance against F. tucumaniae was evaluated in light of the Disease index (DX) values from the recombinant inbred lines (RIL) and from he genotypes derived from the residual heterozygous line (RHL), RH1-73

  • (1)S: homozygous for the susceptible genotype; R: homozygous for resistant genotype estimated by flanking markers. (2)The number of plants tested for re-evaluation in Japan (2003)

  • Four quantitative trait loci (QTL) associated with soybean response to sudden death syndrome (SDS), caused by Fusarium tucumaniae, are located at linkage groups a1, k, and i

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Summary

Introduction

Soybean sudden death syndrome (SDS) due to the closely related soil-borne fungi Fusarium solani f. sp. phaseoli (Roy et al, 1989; Rupe, 1989; O’Donnell & Gray, 1995; Achenbach et al, 1996) and F. solani f. sp. glycines (Rupe, 1989; Roy, 1997) results in severe field losses of soybean in the U.S (Wrather et al, 1995, 1997), Argentina, and Brazil (Rupe & Hartman, 1999).A major resistance gene to F. solani f. sp. glycines, Rfs, was divided into Rfs, the gene for resistance to root infection, and Rft, the gene for resistance to leaf symptoms (Meksem et al, 1999). 'Forrest', and an evaluation of leaf symptoms, it is known that quantitative resistance to SDS is derived from a 'Forrest' allele in a region of linkage group g and an 'Essex' allele in a region of linkage group c2 (Chang et al, 1996). Three additional QTL for resistance to SDS (one in each linkage groups g, n, and c2) were identified by using RIL derived from 'Pyramid' × 'Douglas' (Njiti et al, 2002). These loci convey resistance against SDS; in South America, SDS is caused by Fusarium tucumaniae sp. These loci convey resistance against SDS; in South America, SDS is caused by Fusarium tucumaniae sp. nov., which is phylogenetically and morphologically different from Fusarium virguliforme sp. nov. (synonymous with F. solani f. sp. glycines), the causative agent of SDS in North America (Aoki et al, 2003)

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