Mapping of the Frl Locus Conferring Resistance to Fusarium oxysporum f.sp. radicis-lycopersici(FORL) in Tomato and Identification of RAPD Markers Linked to a New Source of Resistance

Fusarium crown and root rot of tomato is caused by Fusarium oxysporum f.sp. radicis-lycopersici (FORL). A single dominant gene ( Frl) derived from L. peruvianum L. (Mill.) was previously identified as a useful source of resistance to FORL. The objective of this research was to identify molecular markers linked to Frl and RAPD markers linked to a new source of resistance to FORL being developed from L. pennellii (Corr.) D'Arcy accession LA1277. The DNAs of resistant ( Frl) and susceptible breeding lines were screened for polymorphisms using 1200 RAPD primers. Of these, only 104 yielded polymorphisms between the resistant and susceptible lines. These polymorphisms were then tested on four additional tomato lines homozygous for Frl and an additional pair of near-isogenic lines developed by Dr. Laterrot. Only 13 primers still produced consistent polymorphisms between all resistant and susceptible lines. Four of these polymorphisms (RAPD 116, 194, 405, 655) were determined to be linked to Frl in an F 5 segregating population using an inoculation procedure devised to clearly differentiate susceptible and resistant plants. The linkage between ah and Frl reported by Laterrot [Laterrot and Moretti Tomato Genet. Coop. Rep. 45:29 (1995)] places Frl on the long arm of chromosome 9 of the tomato genome. The parent lines were also tested with a sequence tagged site (STS) of TG101, which is tightly linked to Tm2 a [Young et al., Genetics 120:579-585 (1988)] and yielded polymorphic codominant bands. This STS was also tested on the F 5 segregating population and it cosegregated with the resistance and with the RAPD markers. Breeding of the second source of resistance is still in progress. The DNAs of 30 resistant BC 1 F 5 plants derived from LA1277 were bulked and compared to the recurrent susceptible parent DNA using 800 RAPD primers. Of the 800 RAPD primers, 72 yielded consistent polymorphisms. None of the 72 primers were found to produce polymorphisms similar to those identified from the analysis of Frl, thus suggesting the possibility different genetic control being involved with FORL resistance from LA1277.