QTL analyses of two bi-parental mapping populations with AC Barrie as a parent revealed numerous FHB-resistance QTL unique to each population and uncovered novel variation near Fhb1. Fusarium head blight (FHB) is a destructive disease of wheat worldwide, leading to severe yield and quality losses. The genetic basis of native FHB resistance was examined in two populations: a recombinant inbred line population from the cross Cutler/AC Barrie and a doubled haploid (DH) population from the cross AC Barrie/Reeder. Numerous QTL were detected among the two mapping populations with many being cross-specific. Photoperiod insensitivity at Ppd-D1 and dwarfing at Rht-B1 and Rht-D1 was associated with increased FHB susceptibility. Anthesis date QTL at or near the Vrn-A1 and Vrn-B1 loci co-located with major FHB-resistance QTL in the AC Barrie/Reeder population. The loci were epistatic for both traits, such that DH lines with both late alleles were considerably later to anthesis and had reduced FHB symptoms (i.e., responsible for the epistatic interaction). Interestingly, AC Barrie contributed FHB resistance near the Fhb1 locus in the Cutler population and susceptibility in the Reeder population. Analyses of the Fhb1 candidate genes PFT and TaHRC confirmed that AC Barrie, Cutler, and Reeder do not carry the Sumai-3 Fhb1 gene. Resistance QTL were also detected at the expected locations of Fhb2 and Fhb5. The native FHB-resistance QTL detected near Fhb1, Fhb2, and Fhb5 do not appear to be as effective as Fhb1, Fhb2, and Fhb5 from Sumai-3. The presence of awns segregated at the B1 awn inhibitor locus in both populations, but was only associated with FHB resistance in the Cutler/AC Barrie population suggesting linkage caused the association rather than pleiotropy.