Fusarium head blight (FHB) is a serious disease of wheat. Robertsonian translocation 7DS.7el2L wheat (Triticum aestivum L.) line KS24-2 was characterized as having FHB resistance. The long arm of chromosome 7el2 likely has agronomic undesirable genes. Our objective is to reduce the amount of 7el2L chromatin, yet retain the FHB resistance. The gene(s) for resistance to FHB is near the distal region of the long arm of 7el2. KS24-2 was crossed to a genetic line of wheat cv. Chinese Spring, in which the Ph locus on chromosome 5B was deleted, so that there is induced homeologous pairing and recombination during meiosis in plants that are homozygous for the Ph deletion (genotype phph). We identified F2 seedlings that were phph using the STS marker WPG90. Among the phph F2 plants, we selected translocation heterozygotes using two markers; gwm333 which is dominant and specific for 7el2, and gdm150 which is dominant and specific for 7D. Aproximately 15 plants each of 17 F3 families were phenotyped for FHB resistance by inoculating a single basal floret of the third spikelet from the tip of primary spikes at flowering with 10 µl of aqueous inoculum containing 500-1,000 conidia spores of a local isolate of Fusarium graminearum, and recording disease spread at 21 d after inoculation as the number of diseased spikelets, an indication of type II resistance. Resistant plants were genotyped for markers located along 7DL/7el2L and one plant lost the marker Xgwm333-7el2, but retained the 7el2-specific marker loci of the distal half of the 7el2L segment, as revealed with Xpsr129, BE445567, and Xcfa2240. These three markers were associated by segregation analysis with the FHB resistance in a backcross population. We suggest that the7el2L segment of this wheat line is shorter than that of the donor translocation line KS24-2, but the FHB resistance is retained.