RFLP-based analysis of recombination among resistance genes to fusarium wilt races 1, 2, and 3 in tomato

Tomato (Lycopersicon esculentum) line E427 has resistance genes to all three races of Fusarium oxysporum f.sp. lycopersici derived from L. pennellii accession LA 716 and L. pimpinellifolium accession PI 126915. To determine genes that confer resistance to specific races of fusarium wilt, line E427 was crossed to susceptible 'Bonny Best' and then F₂ and backcross (to 'Bonny Best') seed were obtained. Self-pollinations resulted in 337 lines and progeny of each line was inoculated separately with fusarium wilt races 1, 2, or 3. Plants from lines whose segregation suggested recombination of resistance were self-pollinated and reinoculated until disease reactions were homozygous. Four lines were obtained with resistance to both races 2 and 3, but susceptible to race 1. These lines had the L. pennellii alleles at restriction fragment length polymorphism (RFLP) markers linked to I-3 on chromosome 7 and lacked L. pimpinellifolium alleles linked to I and I-2 on chromosome 11. Complementation (F₂) data indicated race 2 resistance on chromosome 7 was controlled by a single dominant gene. Three lines were resistant to race 2, but susceptible to races 1 and 3. These lines had L. pimpinellifolium alleles at TG105 and flanking markers encompassing a 14.4 cM region indicating the presence of I-2, and no L. pennellii alleles at markers linked to I-3. Three lines were resistant to race 1, but susceptible to races 2 and 3. All three lines had L. pimpinellifolium alleles at TG523 confirming linkage to I on chromosome 11 and no L. pennellii alleles at markers tightly linked to I-3. However, one of the lines, 415, had L. pennellii alleles at CT113 on chromosome 7. This data along with F₂ complementation data suggests the possible existence of a second race 1 resistant locus, 11, in this region. The four lines resistant to both races 2 and 3 were backcrossed again to 'Bonny Best' and self-pollinated progeny from 174 plants were screened as described above. Two lines derived from different BC₁S₁ lines that were fusarium wilt race 3 resistant and susceptible to race 1 had intermediate resistance to race 2. These two lines did not have the L. pennellii alleles at TG183, TG174, and CT43 near the I-3 locus indicating crossovers in this region resulted in reduced race 2 resistance. Collectively, this is the first clear break in the fusarium wilt race 2 and race 1 resistance linkage on chromosome 11. It appears that the race 1 resistance derived from PI 126915 is controlled by the I gene. On chromosome 7, there was a break between the I-3 and I1 genes indicating I-3 does not confer race 1 resistance. The crossovers resulting in reduced resistance to race 2 could be within a complex I-3 locus or a tightly linked race 2 locus.