Plant breeders would welcome new tools to improve selection efficiency for complex traits such as improved flavor, especially since this is only one of many complex traits that a breeder has to integrate into improved cultivars. Using tomato (Lycopersicon esculentum Mill.) flavor as an example, a major obstacle to improvement is the lack of measurable traits to select for. It has been suggested that improved flavor can be achieved by increasing the soluble solids and acidity. Both of these traits are not simply inherited, but if fruit sampling is adequate, they can be measured and selected. Studies have located several molecular markers linked to high soluble solids, but some are also linked to undesirable traits such as small fruit size or low yield. Thus, the molecular markers are not being used in breeding programs at this point. Moreover, other studies have shown that flavor is also influenced by an array of aromatic volatiles. The importance of some of the volatiles has been reported, but the volatile profile that consistently results in superior tomato flavor is still not known. Molecular manipulation of a biochemical pathway has been done to increase the concentration of one volatile with positive results. However, this manipulation does not solve the overall flavor improvement problem. Furthermore, environment plays a profound role in tomato flavor, and this aspect needs to be dealt with if a branded high-quality product is to be successfully marketed. There are also flavor issues related to fruit firmness, pedicel type, and plant habit. In summary, molecular techniques may be useful in providing some incremental improvements for complex traits like tomato flavor, but more knowledge about targets to manipulate is required. There does not appear to be any cheap or easy solutions. If molecular approaches are to be commercially successful, they will have to be tied closely to a breeding program dedicated to the same goal.
Two hundred eight-four Lycopersicon spp. genotypes reported to have some resistance to bacterial pathogens of tomato (L. esculentum Mill.) were inoculated in the field with Xanthomonas campestris pv. vesicatoria (XCV), the incitant of bacterial spot, and rated for disease severity in summer 1982 and/or summer 1983. One line tested in 1983, Hawaii 7998, had no definite XCV lesions and later was determined to be resistant to XCV in the laboratory. Genotypes with the highest levels of resistance during 2 years of testing were: Ohio 4013-3, Ohio 4014-4, Heinz 1568-F3, [(Subarctic Delite × MH1) × H603] F5, L556, ‘Campbell-28’, PI 127813, Heinz 603-F11, PI 224573, ‘Monense’, ‘Heinz 2990’, and PI 324708. Genotypes with highest levels of resistance in one year of testing were PI 379032 and ‘Burgess Crack Proof. In 1982, PI 270248- ‘Sugar’ had a high level of resistance to XCV on fruit, but foliage was susceptible.
Lycopersicon pennellii accession LA 1277 was crossed to tomato (L. esculentum) and the F1 was backcrossed to tomato. Self-pollinated seed was saved from backcross plants and seedlings derived were inoculated with Fusarium oxysporum Schlecht f.sp. radicus-lycopersici Jarvis and Shoemaker, the causal agent of Fusarium crown and root rot (FCRR). Seed was saved from resistant plants that were self-pollinated and screened until homozygous resistance was verified five generations after the backcross. Three homozygous lines were crossed to Fla. 7547, a tomato breeding line susceptible to FCRR but resistant to Fusarium wilt races 1, 2, and 3. Subsequently, backcrosses were made to each parent and F2 seed were obtained. The three homozygous FCRR-resistant lines were also crossed to Ohio 89-1, which has a dominant gene for FCRR resistance presently being used in breeding programs. F2 seed were obtained from these crosses. These generations were inoculated with the FCRR pathogen. The resistant parents, F1, and backcross to the resistant parents were all healthy. The backcross to the susceptible parent and the F2 segregated healthy to susceptible plants in 1:1 and 3:1 ratios, respectively. Thus, the resistance from LA 1277 was inherited as a single dominant gene. This gene was different than the gene from Ohio 89-1 because susceptible segregants were detected in the F2 generation derived from the two resistant sources.
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.
The genetic basis of resistance to tomato yellow leaf curl virus (TYLCV) and tomato mottle virus (ToMoV) was studied in three different mapping populations of tomato (Lycopersicon esculentum Mill.). Bulked segregant analysis (BSA) was used to identify random amplification of polymorphic DNA (RAPD) markers linked to TYLCV and ToMoV resistance. Segregated RAPD markers associated with resistance were linked to morphological markers self-pruning (sp) and potato leaf (c) on chromosome 6. RAPD genetic linkage maps of chromosome 6 were constructed for each of the three populations. Common mapped markers revealed straightforward homologies between the chromosome 6 linkage group of the three populations. Multiple-QTL mapping (MQM) was used to identify quantitative trait loci (QTL) for resistance linked to chromosome 6. These revealed that the resistance against TYLCV and ToMoV was mainly explained by two QTL in two populations and one QTL in another. For all of the resistance QTL detected, the favorable allele was provided by the resistant parents. The presence of three different sources of TYLCV and ToMoV resistance, and the markers in tight linkage with them, provide a means of systemically combining multiple resistance genes. Successful cloning of the R gene from tomatoes would lead to deeper understanding of the molecular basis of resistance to TYLCV and ToMoV, and might also shed light on the evolution of resistance genes in plants in general.
Tomato mottle virus (ToMoV) is a silverleaf whitefly (Bemisia argentifolii Bellows and Perring n. sp.) transmitted, bipartite geminivirus that infects tomatoes (Lycopersicon esculentum Mill.). Inbred lines resistant to ToMoV were derived from Lycopersicon chilense Dunal accession LA 1932. Inheritance was studied using a family developed from the crossing of a resistant inbred with a susceptible tomato inbred over two seasons. The F1 had resistance intermediate to the parents and generation means analysis of F1 and F2, backcross and parental populations suggested that the action of at least two additive genes with high heritability (h2n.s. = 0.87) controlled ToMoV resistance. When data from the two seasons were combined, an acceptable fit to an additive-dominance genetic model was obtained. Single plant comparisons, bulk comparisons, and tailends of F2 populations segregating for ToMoV resistance derived from LA 1932 identified randomly amplified polymorphic DNA (RAPD) markers using eight hundred 10-mer oligonucleotide primers. The F2 populations used for inheritance studies were screened for polymorphic markers, and 12 RAPD markers associated with the ToMoV resistant line were linked to the morphological markers self-pruning (sp) and potato leaf (c) on chromosome 6. RAPD markers that were associated with ToMoV resistance segregated into two linked regions flanking either side of the sp and c loci. The molecular studies suggested that the action of at least two additive regions controlled ToMoV resistance which supported the inheritance analysis.
Heritabilities (h2) and genetic correlations between percent fruit set, yield, and fruit weight were estimated from one summer planting each in Florida and Puerto Rico of 100 S, tomato (Lycopersicon esculentum Mill.) families from a synthetic population. Single-location h2 was high for all traits. Across-locations h2 was low for yield, intermediate for fruit set, and high for fruit weight. Genotype × environment interaction (G × E) was 1) the only significant component of variance for yield, 2) somewhat important for fruit set, and 3) not an important variance component for fruit weight. The greater importance of genetic variance compared to G × E variance explains why across-location heritabilities for fruit weight and fruit set were high. Genetic correlations between fruit set and weight were strongly negative, while those between yield and set were large and positive. Yields under high temperatures may increase with selection for fruit set, but a reduction in fruit weight would be expected in this population and those with similar genetic correlations.