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pubmed-article:8434613pubmed:abstractTextThe absence of recombination between the mutation causing Friedreich ataxia and the two loci which originally assigned the disease locus to chromosome 9 has slowed attempts to isolate and characterize the genetic defect underlying this neurodegenerative disorder. A proximity of less than 1 cM to the linkage group has been proved by the generation of high maximal lod score (Z) to each of the two tightly linked markers D9S15 (Z = 96.69; recombination fraction [theta] = .01) and D9S5 (Z = 98.22; theta = .01). We report here recombination events which indicate that the FRDA locus is located centromeric to the D9S15/D9S5 linkage group, with the most probable order being cen-FRDA-D9S5-D9S15-qter. However, orientation of the markers with respect to the centromere, critical to the positional cloning strategy, remains to be resolved definitively.lld:pubmed
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pubmed-article:8434613pubmed:articleTitleGenetic recombination events which position the Friedreich ataxia locus proximal to the D9S15/D9S5 linkage group on chromosome 9q.lld:pubmed
pubmed-article:8434613pubmed:affiliationDepartment of Biochemistry and Molecular Genetics, St. Mary's Hospital Medical School, London, England.lld:pubmed
pubmed-article:8434613pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8434613pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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