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VIEW ARTICLE   |    DOI: 10.1094/MPMI-7-0464


Genetic Dissection of Oligogenic Resistance to Bacterial Wilt in Tomato. Dariush Danesh. Department of Plant Pathology, 495 Borlaug Hall, University of Minnesota, St. Paul 55108 U.S.A. Sharon Aaarons, Gail E. McGill, and Nevin D. Young. Department of Plant Pathology, 495 Borlaug Hall, University of Minnesota, St. Paul 55108 U.S.A. MPMI 7: 464-471. Accepted 7 April 1994. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1994.


To study resistance to bacterial wilt (caused by Pseudomonas solanacearum) in tomato, we analyzed 71 F2, individuals from a cross between a resistant and a susceptible parent with 79 DNA markers. F2 plants were inoculated by two methods: bacteria were injected into schoots of cuttings or poured into soil surrounding wounded roots. Disease responses were scored on a scale of 0 to 5. Statistical comparisons between DNA marker genotypes and disease phenotypes identified three genomic regions correlated with resistance. In plants inoculated through roots, genomic regions on chromosomes 6 and 10 were correlated with resistance. In plants inoculated through shoots, a region on chromosome 7 was significant, as were the regions on chromosomes 6 and 10. The relative impact of resistance loci on disease response difered between shoot and root inoculations. To confirm the existence of a partial resistance gene on chromosome 6, an F2 individual homozygous for the resistant parent's alleles on chromosomes 7 and 10, but heterozygous for markers on chromosome 6, was selfed. Analysis of the F3 progeny confirmed that a partial resistance locus was located on chromosome 6, very close to CT184. The presence of a partial resistance locus on chromosome 10 was similarly confirmed by analysis of progeny of another F2 plant chosen on the basis of its marker phenotype.

Additional Keywords: genetic mapping, host-microbe interactions, partial disease resistance, polygenic, quantitative trait loci, restriction fragment length polymorphism.