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Quantitative trait loci underlying resistance to sudden death syndrome (SDS) in MD96-5722 by ‘ Spencer ’ recombinant inbred line population of soybean

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ABSTRACT

The best way to protect yield loss of soybean [Glycine max (L.) Merr.] due to sudden death syndrome (SDS), caused by Fusarium virguliforme (Aoki, O’Donnel, Homma & Lattanzi), is the development and use of resistant lines. Mapping quantitative trait loci (QTL) linked to SDS help developing resistant soybean germplasm through molecular marker-assisted selection strategy. QTL for SDS presented herein are from a high-density SNP-based genetic linkage map of MD 96-5722 (a.k.a ‘Monocacy’) by ‘Spencer’ recombinant inbred line using SoySNP6K Illumina Infinium BeadChip genotyping array. Ninety-four F5:7 lines were evaluated for 2 years (2010 and 2011) at two locations (Carbondale and Valmeyer) in southern Illinois, USA to identify QTL controlling SDS resistance using disease index (DX). Composite interval mapping identified 19 SDS controlling QTL which were mapped on 11 separate linkage group (LG) or chromosomes (Chr) out of 20 LG or Chr of soybean genome. Many of these significant QTL identified in one environment/year were confirmed in another year or environment, which suggests a common genetic effects and modes of the pathogen. These new QTL are useful sources for SDS resistance studies in soybean breeding, complementing previously reported loci.

No MeSH data available.


Phenotypic distribution of mean values of disease index (DX) from three different growing environments (Carbondale, IL in 2010 and Valmeyer, IL in 2010 and 2011) of MD 96-5722 and ‘Spencer’ recombinant inbred line (RIL) population. Mean values and standard deviation (mean ± SD) of DX, skewness and kurtosis are shown at the lower part of figure
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Fig1: Phenotypic distribution of mean values of disease index (DX) from three different growing environments (Carbondale, IL in 2010 and Valmeyer, IL in 2010 and 2011) of MD 96-5722 and ‘Spencer’ recombinant inbred line (RIL) population. Mean values and standard deviation (mean ± SD) of DX, skewness and kurtosis are shown at the lower part of figure

Mentions: Frequency distribution of DX was nearly normal as skewness and kurtosis values were <1.00 (Fig. 1). Mean squares of environment (E), replication (R), and genotype (G) were significant at P ≤ 0.0001, while G × E interaction was significant at P ≤ 0.005 for DX (Table 1). DX variation was 47.9 % and heritability was as low as 0.20, which is probably the consequence of high environmental variances (Table 2).Fig. 1


Quantitative trait loci underlying resistance to sudden death syndrome (SDS) in MD96-5722 by ‘ Spencer ’ recombinant inbred line population of soybean
Phenotypic distribution of mean values of disease index (DX) from three different growing environments (Carbondale, IL in 2010 and Valmeyer, IL in 2010 and 2011) of MD 96-5722 and ‘Spencer’ recombinant inbred line (RIL) population. Mean values and standard deviation (mean ± SD) of DX, skewness and kurtosis are shown at the lower part of figure
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4362743&req=5

Fig1: Phenotypic distribution of mean values of disease index (DX) from three different growing environments (Carbondale, IL in 2010 and Valmeyer, IL in 2010 and 2011) of MD 96-5722 and ‘Spencer’ recombinant inbred line (RIL) population. Mean values and standard deviation (mean ± SD) of DX, skewness and kurtosis are shown at the lower part of figure
Mentions: Frequency distribution of DX was nearly normal as skewness and kurtosis values were <1.00 (Fig. 1). Mean squares of environment (E), replication (R), and genotype (G) were significant at P ≤ 0.0001, while G × E interaction was significant at P ≤ 0.005 for DX (Table 1). DX variation was 47.9 % and heritability was as low as 0.20, which is probably the consequence of high environmental variances (Table 2).Fig. 1

View Article: PubMed Central

ABSTRACT

The best way to protect yield loss of soybean [Glycine max (L.) Merr.] due to sudden death syndrome (SDS), caused by Fusarium virguliforme (Aoki, O&rsquo;Donnel, Homma &amp; Lattanzi), is the development and use of resistant lines. Mapping quantitative trait loci (QTL) linked to SDS help developing resistant soybean germplasm through molecular marker-assisted selection strategy. QTL for SDS presented herein are from a high-density SNP-based genetic linkage map of MD 96-5722 (a.k.a &lsquo;Monocacy&rsquo;) by &lsquo;Spencer&rsquo; recombinant inbred line using SoySNP6K Illumina Infinium BeadChip genotyping array. Ninety-four F5:7 lines were evaluated for 2&nbsp;years (2010 and 2011) at two locations (Carbondale and Valmeyer) in southern Illinois, USA to identify QTL controlling SDS resistance using disease index (DX). Composite interval mapping identified 19 SDS controlling QTL which were mapped on 11 separate linkage group (LG) or chromosomes (Chr) out of 20 LG or Chr of soybean genome. Many of these significant QTL identified in one environment/year were confirmed in another year or environment, which suggests a common genetic effects and modes of the pathogen. These new QTL are useful sources for SDS resistance studies in soybean breeding, complementing previously reported loci.

No MeSH data available.