Abstract Fusarium oxysporum f. sp. batatas , the causal agent of Fusarium wilt disease, was once the most damaging pathogen of sweetpotato in the United States. Breeding for cultivar resistance has largely addressed this issue, however, little is known about the genetic basis for resistance. Historically, sweetpotato breeders have relied on the high heritability of Fusarium wilt resistance, so identification of a region controlling resistance would be a major first step in implementing marker‐assisted selection for this trait. We assayed a biparental mapping population, NCDM04‐0001 × ‘Covington’ (DC), consisting of a susceptible by resistant cross composed of 454 progenies, for resistance to Fusarium wilt disease using visual assessments and an ordinal disease severity rating scale. Parental and check lines performed as expected, and the DC population exhibited segregation for resistance across trials over 3 years and in a joint analysis. We next performed quantitative trait locus (QTL) analyses using a linkage map based on the Ipomoea trifida diploid reference genome. Across multiple trials, we repeatedly detected a major QTL on chromosome 10, herein named qIbFo‐10.1. This QTL had a heritability of 33.8%, suggesting that a single locus explains a large amount of variation for resistance to this critically important trait. A basic local alignment search tool revealed several candidate genes: itf10g19820 (transcriptional factor B3 family protein/auxin‐responsive factor AUX/IAA‐related), four LRR‐kinases (leucine‐rich repeat receptor kinase) (itf10g21910, itf10g19200, itf10g19260, and itf10g20000), and two toll‐interleukin‐resistance genes (itf10g20200 and itf10g20220). Future efforts should develop molecular tools for Fusarium wilt resistance breeding, resulting in shorter breeding cycles and faster variety releases.
Fraher et al. (Thu,) studied this question.