Soybean Sudden Death Syndrome Resistance Research Articles

Genome wide association study identifies novel single nucleotide polymorphic loci and candidate genes involved in soybean sudden death syndrome resistance.

Fusarium virguliforme is a soil borne root pathogen that causes sudden death syndrome (SDS) in soybean [Glycine max (L.) Merrill]. Once the fungus invades the root xylem tissues, the pathogen secretes toxins that cause chlorosis and necrosis in foliar tissues leading to defoliation, flower and pod drop and eventually death of plants. Resistance to F. virguliforme in soybean is partial and governed by over 80 quantitative trait loci (QTL). We have conducted genome-wide association study (GWAS) for a group of 254 plant introductions lines using a panel of approximately 30,000 SNPs and identified 19 single nucleotide polymorphic loci (SNPL) that are associated with 14 genomic regions encoding foliar SDS and eight SNPL associated with seven genomic regions for root rot resistance. Of the identified 27 SNPL, six SNPL for foliar SDS resistance and two SNPL for root rot resistance co-mapped to previously identified QTL for SDS resistance. This study identified 13 SNPL associated with eight novel genomic regions containing foliar SDS resistance genes and six SNPL with five novel regions for root-rot resistance. This study identified five genes carrying nonsynonymous mutations: (i) three of which mapped to previously identified QTL for foliar SDS resistance and (ii) two mapped to two novel regions containing root rot resistance genes. Of the three genes mapped to QTL for foliar SDS resistance genes, two encode LRR-receptors and third one encodes a novel protein with unknown function. Of the two genes governing root rot resistance, Glyma.01g222900.1 encodes a soybean-specific LEA protein and Glyma.10g058700.1 encodes a heparan-alpha-glucosaminide N-acetyltransferase. In the LEA protein, a conserved serine residue was substituted with asparagine; and in the heparan-alpha-glucosaminide N-acetyltransferase, a conserved histidine residue was substituted with an arginine residue. Such changes are expected to alter functions of these two proteins regulated through phosphorylation. The five genes with nonsynonymous mutations could be considered candidate SDS resistance genes and should be suitable molecular markers for breeding SDS resistance in soybean. The study also reports desirable plant introduction lines and novel genomic regions for enhancing SDS resistance in soybean.

Different loci associated with root and foliar resistance to sudden death syndrome (Fusarium virguliforme) in soybean.

Different loci associated with root resistance to F. virguliforme colonization and foliar resistance to phytotoxin damage in soybean. Use of resistant cultivars is the most efficacious approach to manage soybean sudden death syndrome (SDS), caused by Fusarium virguliforme. The objectives of this study were to (1) map the loci associated with root and foliar resistance to F. virguliforme infection and (2) decipher the relationships between root infection, foliar damage, and plot yield. A mapping population consisting of 153 F4-derived recombinant inbred lines from the cross U01-390489 × E07080 was genotyped by SoySNP6K BeadChip assay. Both foliar damage and F. virguliforme colonization in roots were investigated in the field, and a weak positive correlation was identified between them. Foliar damage had a stronger negative correlation with plot yield than F. virguliforme colonization. Twelve loci associated with foliar damage were identified, and four of them were associated with multiple traits across environments. In contrast, only one locus associated with root resistance to F. virguliforme colonization was identified and mapped on Chromosome 18. It colocalized with the locus associated with foliar damage in the same environment. The locus on Chromosome 6, qSDS6-2, and the locus on Chromosome 18, qSDS18-1, were associated with resistance to SDS phytotoxins and resistance to F. virguliforme colonization of roots, respectively. Both loci affected plot yield. Foliar damage-related traits, especially disease index, are valuable indicators for SDS resistance breeding because of consistency of the identified loci and their stronger correlation with plot yield. The information provided by this study will facilitate marker-assisted selection to improve SDS resistance in soybean.

Temporal Dynamics of Fusarium virguliforme Colonization of Soybean Roots.

Soybean sudden death syndrome (SDS) caused by Fusarium virguliforme is one of the most yield limiting soybean diseases in the United States. SDS disease symptoms include root rot and foliar symptoms induced by fungal toxins. Soybean cultivar resistance is one of the most effective SDS disease management options, but no cultivar displays complete resistance. Soybean SDS foliar symptoms are the primary phenotype used to screen and breed for SDS resistance. Root rot or root colonization measures are seldom utilized, partly due to the lack of convenient and accurate methods for quantification of F. virguliforme. In this study, greenhouse and field experiments were conducted to determine the temporal dynamics of F. virguliforme colonization of soybean roots using quantitative real-time PCR (qPCR). The infection coefficient (IC), or ratio of F. virguliforme DNA to soybean DNA, was determined in soybean cultivars with different SDS foliar resistance ratings. In greenhouse experiments, F. virguliforme was detected in all cultivars 7 days after planting (DAP), with a peak in IC at 14 DAP. All soybean cultivars developed SDS foliar symptoms, but F. virguliforme soybean root colonization levels did not significantly correlate with SDS foliar symptom severity. In field experiments, SDS foliar symptoms developed among soybean cultivars in alignment with provided foliar resistance ratings; however, the F. virguliforme IC were not significantly different between SDS foliar symptomatic and asymptomatic cultivars. F. virguliforme was detected in all cultivars at the first sample collection point 25 DAP (V3 vegetative growth stage), and the IC increased throughout the season, peaking at the last sample collection point 153 DAP (postharvest). Collectively, appearance and disease severity ratings of SDS foliar symptoms were not associated with F. virguliforme quantity in roots, suggesting a need to include F. virguliforme root colonization in breeding efforts to screen soybean germplasm for F. virguliforme root infection resistance. The findings also demonstrates root colonization of the pathogen on nonsymptomatic soybean cultivars leading to persistence of the pathogen in the field, and possible hidden yield loss.

Integration of sudden death syndrome resistance loci in the soybean genome.

Complexity and inconsistencies in resistance mapping publications of soybean sudden death syndrome (SDS) result in interpretation difficulty. This review integrates SDS mapping literature and proposes a new nomenclature system for reproducible SDS resistance loci. Soybean resistance to sudden death syndrome (SDS) is composed of foliar resistance to phytotoxins and root resistance to pathogen invasion. There are more than 80 quantitative trait loci (QTL) and dozens of single nucleotide polymorphisms (SNPs) associated with soybean resistance to SDS. The validity of these QTL and SNPs is questionable because of the complexity in phenotyping methodologies, the disease synergism between SDS and soybean cyst nematode (SCN), the variability from the interactions between soybean genotypes and environments, and the inconsistencies in the QTL nomenclature. This review organizes SDS mapping results and proposes the Rfv (resistance to Fusarium virguliforme) nomenclature based on supporting criteria described in the text. Among ten reproducible loci receiving our Rfv nomenclature, Rfv18-01 is mostly supported by field studies and it co-localizes to the SCN resistance locus rhg1. The possibility that Rfv18-01 is a pleiotropic resistance locus and the concern about Rfv18-01 being confounded with Rhg1 is discussed. On the other hand, Rfv06-01, Rfv06-02, Rfv09-01, Rfv13-01, and Rfv16-01 were identified both by screening soybean leaves against phytotoxic culture filtrates and by evaluating SDS severity in fields. Future phenotyping using leaf- and root-specific resistance screening methodologies may improve the precision of SDS resistance, and advanced genetic studies may further clarify the interactions among soybean genotypes, F. virguliforme, SCN, and environments. The review provides a summary of the SDS resistance literature and proposes a framework for communicating SDS resistance loci for future research considering molecular interactions and genetic breeding for soybean SDS resistance.

'MN1606SP' by 'Spencer' filial soybean population reveals novel quantitative trait loci and interactions among loci conditioning SDS resistance.

Four novel QTL and interactions among QTL were identified in this research, using as a parent line the most SDS-resistant genotype within soybean cultivars of the US early maturity groups. Soybean sudden death syndrome (SDS) reduces soybean yield in most of the growing areas of the world. The causal agent of SDS, soilborne fungus Fusarium virguliforme (Fv), releases phytotoxins taken up by the plant to produce chlorosis and necrosis in the leaves. Planting resistant cultivars is the most successful management practice to control the disease. The objective of this study was to identify quantitative trait loci (QTL) associated with the resistance response of MN1606SP to SDS. A mapping population of F 2:3 lines created by crossing the highly resistant cultivar 'MN1606SP' and the susceptible cultivar 'Spencer' was phenotyped in the greenhouse at three different planting times, each with three replications. Plants were artificially inoculated using SDS infested sorghum homogeneously mixed with the soil. Data were collected on three disease criteria, foliar disease incidence (DI), foliar leaf scorch disease severity (DS), and root rot severity. Disease index (DX) was calculated as DI × DS. Ten QTL were identified for the different disease assessment criteria, three for DI, four for DX, and three for root rot severity. Three QTL identified for root rot severity and one QTL for disease incidence are considered novel, since no previous reports related to these QTL are available. Among QTL, two interactions were detected between four different QTL. The interactions suggest that resistance to SDS is not only dependent on additive gene effects. The novel QTL and the interactions observed in this study will be useful to soybean breeders for improvement of SDS resistance in soybean germplasm.

The ‘PI 438489B’ by ‘Hamilton’ SNP-Based Genetic Linkage Map of Soybean [Glycine max (L.) Merr.] Identified Quantitative Trait Loci that Underlie Seedling SDS Resistance

Soybeans [Glycine max (L.) Merr.] are susceptible to many diseases including fungal diseases such as soybean sudden death syndrome (SDS). Several studies reported SDS resistance quantitative trait loci (QTL) on the soybean genome using different recombinant inbred line (RIL) populations and low density genetic linkage maps. High density exclusively single nucleotide polymorphisms-based (SNP-based) maps were not yet reported in soybean. The objectives of this study were (1) to construct a high density SNP-based genetic linkage map of soybean using the ‘PI438489B’ by ‘Hamilton’ (PIxH, n=50) recombinant inbred line population, and (2) to map QTL for SDS resistance using this high-density reliable genetic SNP-based map. The PI438489B by Hamilton high-density SNP-based genetic map was a high density map composed of 31 LGs, 648 SNPs, and covered 1,524.7 cM with an average of 2.37 cM between two adjacent SNP markers. Fourteen significant QTL were identified for SDS resistance using interval mapping (IM) and composite interval mapping (CIM) with LOD scores that ranged between 2.6 and 5.0. Twelve QTL were identified for foliar disease severity (FDS) and three QTL for root rot severity (RRS) of which one QTL underlain both FDS and RRS. The fourteen QTL were mapped onto ten separate chromosomes of the soybean genome. Seven of the intervals encompassing the QTL had been identified previously (on LGs C1, C2, D1b, G, L, N and O) associated with resistance to SDS but seven were novel (LGs A2 (2), B1, C2, D1a, D1b and O). We constructed the first PI438489B by Hamilton exclusively SNP-Based map and identified fourteen QTL that underlie SDS resistance including both resistances to foliar and root rot symptoms caused by Fusarium virguliforme infection. The QTL discovered here for SDS resistance could be useful to include in breeding programs in developing soybean cultivars resistant to SDS.

ISOLATION AND CHARACTERIZATION OF Fusarium solani CAUSING SOYBEAN SUDDEN DEATH SYNDROME IN KOREA

Soybean sudden death syndrome (SDS), caused by members of the Fusarium solani species complex, is an important disease leading to substantial yield reductions. The threat of soybean SDS is becoming serious in Korea, probably due to changes in the climate favoring the prevalence of this disease. In this study, after isolating Fusarium spp. from root rot-symptomatic soybean, we determined that F. solani was a causal agent of soybean SDS based on morphological and molecular characterization as well as Koch’s postulate. From 2009 to 2011, a total of nine isolates of Fusarium solani were collected from major soybean fields, Korea. Morphological and TEF-1α sequence analyses confirmed a variety of nine F. solani isolates. All F. solani isolates were close with F. solani species from Asia and mostly belonged to F. solani f. sp. pisi (SSLP14, 15, 16,19, and 20). Based on homology analysis of both ITS and TEF-1α, some isolates (SSLP2, 18, and 22) were similar to F. solani causing human eye keratitis, indicating a shared pathogenicity both on humans and plants. In a pathogenicity test, we observed hyphae in both xylem and phloem tissues from discolored roots and basal stems of plants exhibiting foliar SDS symptoms, indicating its contribution to foliar symptoms. Based on the differential reactions of soybean plant genotypes to F. solani isolates, one indigenous F. solani isolates, SSLP15 was identified having the highest levels of virulence. In addition, Danbaekkong and Jinpumkong 2 soybean were found to be resistant to SDS as demonstrated by slight symptom with less than 20% foliage affected. The evaluation of SDS resistance could be beneficial to support varietal improvement through extensive soybean breeding program in Korea.

Identification of Fusarium virguliforme FvTox1-Interacting Synthetic Peptides for Enhancing Foliar Sudden Death Syndrome Resistance in Soybean.

Soybean is one of the most important crops grown across the globe. In the United States, approximately 15% of the soybean yield is suppressed due to various pathogen and pests attack. Sudden death syndrome (SDS) is an emerging fungal disease caused by Fusarium virguliforme. Although growing SDS resistant soybean cultivars has been the main method of controlling this disease, SDS resistance is partial and controlled by a large number of quantitative trait loci (QTL). A proteinacious toxin, FvTox1, produced by the pathogen, causes foliar SDS. Earlier, we demonstrated that expression of an anti-FvTox1 single chain variable fragment antibody resulted in reduced foliar SDS development in transgenic soybean plants. Here, we investigated if synthetic FvTox1-interacting peptides, displayed on M13 phage particles, can be identified for enhancing foliar SDS resistance in soybean. We screened three phage-display peptide libraries and discovered four classes of M13 phage clones displaying FvTox1-interacting peptides. In vitro pull-down assays and in vivo interaction assays in yeast were conducted to confirm the interaction of FvTox1 with these four synthetic peptides and their fusion-combinations. One of these peptides was able to partially neutralize the toxic effect of FvTox1 in vitro. Possible application of the synthetic peptides in engineering SDS resistance soybean cultivars is discussed.

Genome-wide association and epistasis studies unravel the genetic architecture of sudden death syndrome resistance in soybean.

Soybean [Glycine max (L.) Merr.] is an economically important crop that is grown worldwide. Sudden death syndrome (SDS), caused by Fusarium virguliforme, is one of the top yield-limiting diseases in soybean. However, the genetic basis of SDS resistance, especially with respect to epistatic interactions, is still unclear. To better understand the genetic architecture of soybean SDS resistance, genome-wide association and epistasis studies were performed using a population of 214 germplasm accessions and 31,914 SNPs from the SoySNP50K Illumina Infinium BeadChip. Twelve loci and 12 SNP-SNP interactions associated with SDS resistance were identified at various time points after inoculation. These additive and epistatic loci together explained 24-52% of the phenotypic variance. Disease-resistant, pathogenesis-related and chitin- and wound-responsive genes were identified in the proximity of peak SNPs, including stress-induced receptor-like kinase gene 1 (SIK1), which is pinpointed by a trait-associated SNP and encodes a leucine-rich repeat-containing protein. We report that the proportion of phenotypic variance explained by identified loci may be considerably improved by taking epistatic effects into account. This study shows the necessity of considering epistatic effects in soybean SDS resistance breeding using marker-assisted and genomic selection approaches. Based on our findings, we propose a model for soybean root defense against the SDS pathogen. Our results facilitate identification of the molecular mechanism underlying SDS resistance in soybean, and provide a genetic basis for improvement of soybean SDS resistance through breeding strategies based on additive and epistatic effects.

The Genome Sequence of the Fungal Pathogen Fusarium virguliforme That Causes Sudden Death Syndrome in Soybean

Fusarium virguliforme causes sudden death syndrome (SDS) of soybean, a disease of serious concern throughout most of the soybean producing regions of the world. Despite the global importance, little is known about the pathogenesis mechanisms of F. virguliforme. Thus, we applied Next-Generation DNA Sequencing to reveal the draft F. virguliforme genome sequence and identified putative pathogenicity genes to facilitate discovering the mechanisms used by the pathogen to cause this disease.Methodology/Principal FindingsWe have generated the draft genome sequence of F. virguliforme by conducting whole-genome shotgun sequencing on a 454 GS-FLX Titanium sequencer. Initially, single-end reads of a 400-bp shotgun library were assembled using the PCAP program. Paired end sequences from 3 and 20 Kb DNA fragments and approximately 100 Kb inserts of 1,400 BAC clones were used to generate the assembled genome. The assembled genome sequence was 51 Mb. The N50 scaffold number was 11 with an N50 Scaffold length of 1,263 Kb. The AUGUSTUS gene prediction program predicted 14,845 putative genes, which were annotated with Pfam and GO databases. Gene distributions were uniform in all but one of the major scaffolds. Phylogenic analyses revealed that F. virguliforme was closely related to the pea pathogen, Nectria haematococca. Of the 14,845 F. virguliforme genes, 11,043 were conserved among five Fusarium species: F. virguliforme, F. graminearum, F. verticillioides, F. oxysporum and N. haematococca; and 1,332 F. virguliforme-specific genes, which may include pathogenicity genes. Additionally, searches for candidate F. virguliforme pathogenicity genes using gene sequences of the pathogen-host interaction database identified 358 genes.ConclusionsThe F. virguliforme genome sequence and putative pathogenicity genes presented here will facilitate identification of pathogenicity mechanisms involved in SDS development. Together, these resources will expedite our efforts towards discovering pathogenicity mechanisms in F. virguliforme. This will ultimately lead to improvement of SDS resistance in soybean.

Expression of a Single-Chain Variable-Fragment Antibody Against a Fusarium virguliforme Toxin Peptide Enhances Tolerance to Sudden Death Syndrome in Transgenic Soybean Plants

Plants do not produce antibodies. However, plants can correctly assemble functional antibody molecules encoded by mammalian antibody genes. Many plant diseases are caused by pathogen toxins. One such disease is the soybean sudden death syndrome (SDS). SDS is a serious disease caused by the fungal pathogen Fusarium virguliforme. The pathogen, however, has never been isolated from diseased foliar tissues. Thus, one or more toxins produced by the pathogen have been considered to cause foliar SDS. One of these possible toxins, FvTox1, was recently identified. We investigated whether expression of anti-FvTox1 single-chain variable-fragment (scFv) antibody in transgenic soybean can confer resistance to foliar SDS. We have created two scFv antibody genes, Anti-FvTox1-1 and Anti-FvTox1-2, encoding anti-FvTox1 scFv antibodies from RNAs of a hybridoma cell line that expresses mouse monoclonal anti-FvTox1 7E8 antibody. Both anti-FvTox1 scFv antibodies interacted with an antigenic site of FvTox1 that binds to mouse monoclonal anti-FvTox1 7E8 antibody. Binding of FvTox1 by the anti-FvTox1 scFv antibodies, expressed in either Escherichia coli or transgenic soybean roots, was initially verified on nitrocellulose membranes. Expression of anti-FvTox1-1 in stable transgenic soybean plants resulted in enhanced foliar SDS resistance compared with that in nontransgenic control plants. Our results suggest that i) FvTox1 is an important pathogenicity factor for foliar SDS development and ii) expression of scFv antibodies against pathogen toxins could be a suitable biotechnology approach for protecting crop plants from toxin-induced diseases.

The ‘PI 438489B’ by ‘Hamilton’ SNP-Based Genetic Linkage Map of Soybean [Glycine max (L.) Merr.] Identified Quantitative Trait Loci that Underlie Seedling SDS Resistance

Soybeans [Glycine max (L.) Merr.] are susceptible to many diseases including fungal diseases such as soybean sudden death syndrome (SDS). Several studies reported SDS resistance quantitative trait loci (QTL) on the soybean genome using different recombinant inbred line (RIL) populations and low density genetic linkage maps. High density exclusively single nucleotide polymorphisms-based (SNP-based) maps were not yet reported in soybean. The objectives of this study were (1) to construct a high density SNP-based genetic linkage map of soybean using the ‘PI438489B’ by ‘Hamilton’ (PIxH, n=50) recombinant inbred line population, and (2) to map QTL for SDS resistance using this high-density reliable genetic SNP-based map. The PI438489B by Hamilton high-density SNP-based genetic map was a high density map composed of 31 LGs, 648 SNPs, and covered 1,524.7 cM with an average of 2.37 cM between two adjacent SNP markers. Fourteen significant QTL were identified for SDS resistance using interval mapping (IM) and composite interval mapping (CIM) with LOD scores that ranged between 2.6 and 5.0. Twelve QTL were identified for foliar disease severity (FDS) and three QTL for root rot severity (RRS) of which one QTL underlain both FDS and RRS. The fourteen QTL were mapped onto ten separate chromosomes of the soybean genome. Seven of the intervals encompassing the QTL had been identified previously (on LGs C1, C2, D1b, G, L, N and O) associated with resistance to SDS but seven were novel (LGs A2 (2), B1, C2, D1a, D1b and O). We constructed the first PI438489B by Hamilton exclusively SNP-Based map and identified fourteen QTL that underlie SDS resistance including both resistances to foliar and root rot symptoms caused by Fusarium virguliforme infection. The QTL discovered here for SDS resistance could be useful to include in breeding programs in developing soybean cultivars resistant to SDS.

Resistance locus pyramids alter transcript abundance in soybean roots inoculated with Fusarium solani f.sp. glycines.

Soybean Sudden Death Syndrome (SDS) is caused by Fusarium solani f.sp. glycines (Fsg). Six quantitative trait loci (QTLs), each conferring partial resistance to SDS, have been discovered in an Essex x Forrest recombinant inbred line (RIL) population, but their mode of action is not clear. This study aimed to identify genes (ESTs) whose mRNA transcripts were altered in abundance in soybean roots following inoculation of Fsg. Roots of the soybean variety Forrest (four resistance alleles) were inoculated with Fsg, and 14 days later RNA sequences that were differentially expressed relative to uninoculated roots were enriched using suppression subtraction and differential display. The abundance of these RNAs was quantified in inoculated and non-inoculated roots by macroarray hybridizations. A unigene set of 135 ESTs was identified and used in a further macroarray analysis. The abundance of 28 cDNA fragments was increased more than two-fold in inoculated compared to uninoculated roots of RIL 23 (six resistance alleles). In Forrest and Essex (two resistance alleles), the level of only one mRNA was increased two-fold in inoculated roots compared to the uninoculated roots. In Essex most of the mRNAs analyzed decreased in abundance (61/135 showed a two-fold decrease), while in Forrest most mRNA abundances did not change. Among the 28 cDNAs that revealed a two-fold or higher increase in mRNA abundance in RIL 23, 14% code for proteins known to be involved in plant defense, 21% in metabolism, 14% in cell structure and 4% in transport. Unannotated ESTs accounted for 43% of the genes, and 4% of the sequences were previously unknown. The plant defense-related genes that showed a differential response to Fsg inoculation suggested a role for the phenylproponoid pathway in soybean defense against Fsg. In Essex, genes involved in plant defense, cell wall synthesis, ethylene synthesis and metabolism were expressed at lower levels in inoculated roots. The difference in response between the 2-, 4- and 6-gene pyramids suggests that QTLs for SDS resistance serve to delay symptoms or confer resistance by maintaining or increasing the expression of specific genes after inoculation/infection.

Reaction of soybean cultivars to sudden death syndrome and disease scoring methods for screening resistance

Soybean sudden death syndrome (SDS), caused by Fusarium solani f. sp. glycines, is found in more than 2.0 million hectares of soybean fields in Brazil. Identified for the first time during the 1981/82 crop season, in Sao Gotardo, Minas Gerais; it had already spread to 99 counties in Central and South Brazil by the 1999/2000 crop season, causing an estimated yield loss of US$ 53 million. Since no efficient control measure is yet available , it has been carried out through resistant cultivars. One of the difficulties in selecting resistant cultivars lies on the lack of a reliable source of resistance and of a screening method to distinguish the reactions among cultivars. The objective of this study was to define a criterium for differentiating soybean cultivars reaction to SDS and to find sources of resistance to the disease, based on leaf symptoms. The study included eight soybean cultivars in four replication and were carried out in a greenhouse in two experiments. Plants were inoculated by the colonized toothpick method and assessed 21 days after inoculation , using five different assessment criteria. Results showed that during the determination of the AP % (affected plants percentile ), which revealed the different reactions to SDS among soybean cultivars, the levels of chlorosis were not significantly different from those which took into consideration the incidence of leaf chlorosis or necrosis, regardless of the severity of leaf symptoms. The %AP and the scoring method using a scale of 1 to 5 were the best procedures to assess the reaction of soybean cultivars to SDS through leaf symptoms. Cultivar FT Estrela was used as a highly susceptible standard SDS (%AP = 96.32%). Genotypes PI 567734, PI 520733 and MG/BR 46 (Conquista) were the most resistant to SDS with AP % of 30.79%, 31.30% and 35.34%, respectively. They could be used as a source of SDS resistance in crosses in breeding programs.

Two Additional Loci underlying Durable Field Resistance to Soybean Sudden Death Syndrome (SDS)

Severe losses of soybean [Glycine max (L.) Merr.] grain yield occur as a result of the disease sudden death syndrome (SDS), caused by Fusarium solani (Mart.) Sacc. f. sp. phaseoli (Burk.) Snyd. & Hans., type A. Selection for resistance to SDS is currently the most efficient means of yield protection. This study was undertaken within adapted soybean germplasm to identify and characterize loci underlying useful field resistance to SDS. One hundred eleven polymorphic DNA markers were compared with SDS disease response among 100 recombinant inbred lines derived from a cross between a durably SDS resistant cultivar, ‘Forrest’, and a SDS susceptible cultivar, ‘Essex’. SDS disease incidence (DI) and disease severity (DS) were determined in replicated, F. solani infested field‐test sites during 4 yr encompassing five locations. Four separate chromosomal segments were strongly associated with mean SDS DI across 5 locations (P < 0.001). In a previous report using the same genetic materials tested in the same environments two of these quantitative trait loci (QTL) had been identified. With the further analysis with 40 additional markers, two more QTL were detected. The two new QTL were stably associated with SDS resistance within each of five F. solani infested locations (P < 0.007). These two loci were identified by RAPD markers OI03450 and OG13490 and by OE04450 and OE021000. The alleles that conferred resistance were both derived from Forrest. Jointly, the four QTL accounted for about 65% of total phenotypic variability in mean DI and 50% in mean DS. DNA markers can be used to define alleles conferring resistance to SDS. Selection for the SDS resistance QTL may allow efficient selection of resistant genotypes with good yield potential in F. solani infested fields.