effect. Table 3. Effect of two loci on bacterial spot race T4 foliar disease severity in tomato across four populations and two seasons. Resistance to fusarium wilt race 3 was associated with greater susceptibility to bacterial spot in all populations
Samuel F. Hutton, John W. Scott, and Gary E. Vallad
W. Patrick Wechter, Chandrasekar Kousik, Melanie McMillan, and Amnon Levi
Phytopathology 97 461 469 Zhou, X.G. Everts, K.L. Bruton, B.D. 2010 Race 3, a new and highly virulent race of Fusarium oxysporum f. sp. niveum causing fusarium wilt in watermelon Plant Dis. 94 92 98 Zink, F.W. Thomas, C.E. 1990 Genetics of resistance to
Xin Zhao, Qianru Liu, M. Tatiana Sanchez, and Nicholas S. Dufault
grafted plants could be more evident as watermelon fruit develop. Table 3. Root characteristics of nongrafted and grafted seedless watermelon ‘Melody’ in 2015 and 2016 greenhouse experiments with Fusarium oxysporum f. sp. niveum race 2 inoculation. The
G. Craig Yencho, Kenneth V. Pecota, Jonathan R. Schultheis, Zvezdana-Pesic VanEsbroeck, Gerald J. Holmes, Billy E. Little, Allan C. Thornton, and Van-Den Truong
-knot nematode (RKN) race 3. In greenhouse tests, the resistance is greater than resistant ‘Jewel’ and highly susceptible clones ‘Beauregard’ and ‘Porto Rico’. In tests from 2003, 2004, and 2005, average ratings for RKN egg masses for ‘Covington’ were 0.7 (‘Jewel
J.W. Scott and J.P. Jones
Forty-two Lycopersicon pennellii Corr. D'Arcy accessions, from the Tomato Genetics Stock Center, were inoculated for resistance to Fusarium wilt race 3 at the 3-leaf and cotyledon stage. All were over 90% healthy when inoculated at the 3-leaf stage but had greater disease incidence at the cotyledon stage. Crosses were made between healthy plants within each accession. Using this seed, 39 accessions were 100% healthy and 3 were over 96% healthy when inoculated at either stage. Seventeen F1's with susceptible parents were tested for race 3 and all had over 80% healthy plants. Twenty-two accessions were tested for Fusarium wilt race 1 and race 2. For race 1, 21 were 100% healthy and 1 was 91% healthy, For race 2, 20 were 100% healthy, 1 was 96% healthy, and 1 was 75% healthy. Forty accessions were screened for Fusarium crown rot and Verticillium wilt. For crown rot, LA 1277, LA 1367, and LA 1657 were over 95% healthy, 6 other accessions were over 68% healthy and several others had over 50% healthy plants, All 40 were susceptible to Verticillium wilt race 1. L. pennellii appears to be a good source of resistance to Fusarium sp. but not to Verticillium wilt.
James D. McCreight, Michael E. Matheron, Barry R. Tickes, and Belinda Platts
Three races of Fusarium oxysporum f.sp. lactucae, cause of fusarium wilt of lettuce, are known in Japan, where the pathogen was first observed in 1955. Fusarium wilt first affected commercial U.S. lettuce production in 1990 in Huron, Calif., but did not become a serious problem in the U.S. until 2001 when it reappeared in Huron and appeared in the Yuma, Arizona lettuce production area. Reactions of three fusarium wilt differentials (`Patriot', susceptible to races 1, 2 and 3; `Costa Rica No. 4', resistant to race 1, and susceptible to races 2 and 3; and `Banchu Red Fire', susceptible to races 1 and 3, and resistant to race 2) in a naturally-infected commercial field test and artificially-inoculated greenhouse tests, indicated presence of race 1 in the Yuma lettuce production area. Reactions of these differentials to an isolate from Huron confirmed the presence of race 1 in that area. Consistent with previous results from the U.S. and Japan, `Salinas' and `Salinas 88' were resistant to the Yuma and Huron isolates of race 1, whereas `Vanguard' was highly susceptible. Limited F1 and F2 data indicate that resistance to race 1 in `Costa Rica No. 4' and `Salinas' is recessive. `Calmar' is the likely source of resistance in `Salinas' and `Salinas 88'.
John W. Scott*, Hesham A. Agrama, and John P. Jones
Tomato (Lycopersicon esculentum) line E427 has resistance genes to three races of Fusarium oxysporum f.sp. lycopersici derived from L. pennellii (L.pen) accession LA 716 and L. pimpinellifolium (L.pimp) accession PI 126915. E427 was crossed to susc. Bonny Best and F2 and backcross seed were obtained. Progeny were inoculated separately with Fusarium wilt races 1, 2, or 3. Lines with suspected recombination of resistance were selfed and re-inoculated 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.pen alleles at RFLP markers linked to I-3 on chromosome 7 and lacked L.pimp 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.pimp alleles at TG105 indicating the presence of I-2, and no L.pen alleles at markers linked to I-3. Three lines were resistant to race 1, but susceptible to races 2 and 3. All three had L.pimp alleles at TG523 confirming linkage to I on chromosome 11 and no L.pen alleles at markers tightly linked to I-3. However, one of the lines had L.pen alleles at CT113 on chromosome 7. This and F2 complementation data suggests the possible location of a race 1 resistant locus, I1. Two 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 reduced race 2 resistance.
J.W. Scott, H.A. Agrama, and J.P. Jones
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, I1, 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.
Leigh K. Hawkins, Fenny Dane, Thomas L. Kubisiak, and Billy Rhodes
Fusarium wilt, caused by the soilborne fungus Fusarium oxysporum f.sp. niveum (FON), is a serious disease of the watermelon (Citrullus lanatus). Three races of this pathogen (races 0, 1, and 2) have been identified based on differential pathogenicity assays. Most commercially available cultivars are resistant to races 0 and 1. Inheritance for resistance to these races is thought to be controlled by a single dominant gene. No cultivars are resistant to race 2 and resistance is thought to be a quantitative trait. F2 lines derived from a cross between the Fusarium-resistant Citrullus lanatus PI296341, and the Fusarium-susceptible watermelon cultivar `New Hampshire Midget' were used to generate a RAPD-based map of the Citrullus genome. F2:3 families were assayed in the greenhouse for resistance to races 1 and 2. Those families that were either highly resistant or highly susceptible were used in identifying markers linked to Fusarium wilt resistance. A preliminary map of the Citrullus genome based on random amplified polymorphic DNA (RAPD) markers has been expanded with the inclusion of simple sequence repeats (SSRs), amplified fragment length polymorphisms (AFLPs), and isozymes.
Leigh K. Hawkins, Fenny Dane, Tom Kubisiak, Bill Rhodes, and Bob Jarrett
A linkage map was constructed of the watermelon genome using F2 and F2:3 populations segregating for resistance to race 1 and 2 of Fusarium oxysporum f. sp. niveum (FON 1 and 2). Sixty-four percent of the RAPD primers used in the parents and F1 detected polymorphism. In the F2, 143 polymorphic bands were scored, 60% of which exhibited the expected 3:1 segregation ratio. A 113 cM linkage map was constructed using Mapmaker version 3 and LOD of 4. DNA pools of Fusarium wilt resistant or susceptible F2:3 lines were created and bulked segregant analysis was used to detect molecular markers linked to FON 1 or FON 2 resistance. Four individuals per line were used to confirm linkages and construct an F2:3 linkage map. One large linkage group was detected in both generations. A large proportion of the RAPD and SSR markers were unlinked and many showed segregation distortion. Single-factor ANOVA for each pairwise combination of marker locus and resistance or morphological trait was conducted. RAPD markers with putative linkages to FON 1 and FON 2 and several morphological traits were detected.