Abstract

We report a second major QTL for root-knot nematode resistance in the highly resistant Upland cotton line M-120RNR and show epistasis between two resistant QTLs with different mechanisms conferring resistance. In an earlier study, we identified a major QTL on Chromosome 11 associated with resistance to root-knot nematode in the M-120 RNR Upland cotton line (Gossypium hirsutum L.) of the Auburn 623 RNR source. Herein, we re-evaluated the genetics of the resistance to root-knot nematode in the M-120 RNR×Pima S-6 population by linkage mapping using recently published SSR markers. The QTL analysis detected two regions significantly associated with the resistance phenotype. In addition to the QTL previously identified on Chromosome 11 (qMi-C11), a major QTL was identified on Chromosome 14 (qMi-C14). The resistance locus on qMi-C11 originated from the Clevewilt parent, while the qMi-C14 locus originated from the other resistant parent, Mexico Wild Jack Jones. The qMi-C14 locus had logarithms of odds score of 17 and accounted for 45% of the total phenotype variation in egg production. It was also associated with galling index, but the percent variation explained was only 6%, suggesting that the qMi-C11 locus had a much stronger effect on root gall suppression than egg production, while the qMi-C14 locus had a stronger effect on egg production than galling. The results also suggest that the transgressive segregation observed in the development of Auburn 623 RNR was due to the pyramiding of at least two main effect QTLs as well as an additive-by-additive epistatic effects between the two resistant loci. The SSRs markers tightly linked to the qMi-C11 and qMi-C14 loci will greatly facilitate the improvement of RKN resistance in cotton via marker-assisted breeding.

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