Clavibacter michiganensis subsp. michiganensis is the causal agent of bacterial canker of tomato. The disease was first described in 1910 in Michigan, USA. C. michiganensis subsp. michiganensis (from now on called clavibacter) was initially thought to be a phloem parasite, but was later found to be a xylem-invading bacterium. The host range comprises mainly solanaceous crops such as tomato, pepper, and eggplant. Strains show great variability in virulence and are usually described as being hypervirulent, hypovirulent, or nonvirulent. Clavibacter lacks a type III secretion system, and only a few virulence factors have been experimentally determined from the many putative virulence factors. As the molecular mode of infection by clavibacter is unknown, researchers have avoided intensive work on this organism. Genetic plant mechanisms conferring resistance to clavibacter are apparently complex, and breeders have yet to develop disease-resistant cultivars.
Abiotic and biotic stress factors are the major constrains for the realization of crop yield potential. As climate change progresses, the spread and intensity of abiotic as well as biotic stressors is expected to increase, with increased probability of crops being exposed to both types of stress. Shielding crops from combinatorial stress requires a better understanding of the plant's response and its genetic architecture. In this study, we evaluated resistance to salt stress, powdery mildew and to both stresses combined in tomato, using the Solanum habrochaites LYC4 introgression line (IL) population. The IL population segregated for both salt stress tolerance and powdery mildew resistance. Using SNP array marker data, QTLs were identified for salt tolerance as well as Na ? and Cl -accumulation. Salt stress increased the susceptibility of the population to powdery mildew in an additive manner. Phenotypic variation for disease resistance was reduced under combined stress as indicated by the coefficient of variation. No correlation was found between disease resistance and Na ? and Cl -accumulation under combined stress Most genetic loci were specific for either salt stress tolerance or powdery mildew resistance. These findings increase our understanding of the genetic regulation of responses to abiotic and biotic stress combinations and can provide leads to more efficiently breeding tomatoes and other crops with a high level of disease resistance while maintaining their performance in combination with abiotic stress.
Semi-polar metabolites such as flavonoids, phenolic acids, and alkaloids are very important health-related compounds in tomato. As a first step to identify genes responsible for the synthesis of semi-polar metabolites, quantitative trait loci (QTLs) that influence the semi-polar metabolite content in red-ripe tomato fruit were identified, by characterizing fruits of a population of introgression lines (ILs) derived from a cross between the cultivated tomato Solanum lycopersicum and the wild species Solanum chmielewskii. By analyzing fruits of plants grown at two different locations, we were able to identify robust metabolite QTLs for changes in phenylpropanoid glycoconjugation on chromosome 9, for accumulation of flavonol glycosides on chromosome 5, and for alkaloids on chromosome 7. To further characterize the QTLs we used a combination of genome sequencing, transcriptomics and targeted metabolomics to identify candidate key genes underlying the observed metabolic variation.
OTLs affecting oviposition rate mapped to chromosome 1 (Tv-i) and 12 (Tv-2). F3 lines homozygous for either the L. esculentum allele or the L. hirsutum f. glabratum allele at one or both loci confirmed the effects of Tv-i and Tv-2. The F2 population was also evaluated for segregation of type IV and type VI glandular trichome densities. Two QTLs affecting trichome type IV density (TriIV-i and TriIV-2) and one affecting type VI trichome density (TriJ/I-i) mapped to chromosomes 5, 9 and 1, respectively. These results do not support the hypothesis that the density of type IV trichomes is involved in whitefly resistance.
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