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Common loci underlie field resistance to soybean sudden death syndrome in Forrest, Pyramid, Essex, and Douglas

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Abstract

Soybean [Glycine max (L.) Merr.] sudden death syndrome (SDS) caused by Fusarium solani f. sp. glycines results in severe yield losses. Resistant cultivars offer the most-effective protection against yield losses but resistant cultivars such as ’Forrest’ and ’Pyramid’ vary in the nature of their response to SDS. Loci underlying SDS resistance in ’Essex’ × Forrest are well defined. Our objectives were to identify and characterize loci and alleles that underlie field resistance to SDS in Pyramid×’Douglas’. SDS disease incidence and disease severity were determined in replicated field trials in six environments over 4 years. One hundred and twelve polymorphic DNA markers were compared with SDS disease response among 90 recombinant inbred lines from the cross Pyramid×Douglas. Two quantitative trait loci (QTLs) for resistance to SDS derived their beneficial alleles from Pyramid, identified on linkage group G by BARC-Satt163 (261-bp allele, P=0.0005, R2=16.0%) and linkage group N by BARC-Satt080 (230-bp allele, P=0.0009, R2=15.6%). Beneficial alleles of both QTLs were previously identified in Forrest. A QTL for re- sistance to SDS on linkage group C2 identified by BARC-Satt307 (292-bp allele, P=0.0008, R2=13.6%) derived the beneficial allele from Douglas. A beneficial allele of this QTL was previously identified in Essex. Recombinant inbred lines that carry the beneficial alleles for all three QTLs for resistance to SDS were significantly (P≤0.05) more resistant than other recombinant inbred lines . Among these recombinant inbred lines resistance to SDS was environmentally stable. Therefore, gene pyramiding will be an effective method for developing cultivars with stable resistance to SDS.

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Received: 20 October 1999 / Accepted: 22 May 2001

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Njiti, V., Meksem, K., Iqbal, M. et al. Common loci underlie field resistance to soybean sudden death syndrome in Forrest, Pyramid, Essex, and Douglas. Theor Appl Genet 104, 294–300 (2002). https://doi.org/10.1007/s001220100682

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  • DOI: https://doi.org/10.1007/s001220100682

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