Abstract

ABSTRACTSoybean rust (SBR) is caused by the fungal pathogen Phakopsora pachyrhizi and is considered to be the most destructive foliar disease of soybean [Glycine max (L.) Merr.], with soybean yield losses caused by SBR reported to be as high as 80% in severely diseased fields. Studies indicate that most isolates of P. pachyrhizi overcome at least one of the known resistance genes. Therefore, alternative means of controlling SBR such as non‐host‐specific resistance combined with single‐gene resistance could be beneficial in breeding soybean cultivars for SBR resistance. To identify quantitative trait loci (QTL) conditioning variation in SBR‐induced canopy damage, a ‘Benning’ × PI 416947 recombinant inbred line population was planted for 3 yr under natural and artificial infection with P. pachyrhizi in Attapulgus, GA. Although both Benning and PI 416937 are considered susceptible to SBR (they produced tan lesions when infected with P. pachyrhizi), Benning had a higher canopy severity damage score than PI 416937. Multiple interval mapping QTL models identified four QTL conditioning variation in canopy severity damage across the environments and explained 42% of the total phenotypic variation in canopy severity scores. The four QTL were located on chromosomes 8, 9, 13, and 15, which explained 10, 5, 9, and 17% of the phenotypic variation, respectively. When the canopy severity QTL were aligned with previously identified QTL in SoyBase, three canopy severity QTL colocalized with other partial resistance soybean genes and three with the isoflavone daidzein, the precursor of the phytoalexin glyceollin. Glyceollin is involved in plant disease resistance.

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