The Oligosyndactylism (Os) mutation was induced in 1952 by W. Russell at the Oak Ridge Laboratories by irradiation of a (101xC3H) F1 male mouse. An offspring derived from matings with this male exhibited oligosyndactylism on all feet (Gruneberg 1956). In addition to abnormalities in limb formation, Os/+ animals show a reduction in nephron number with compensatory glomerular hypertrophy (Stewart and Stewart 1969). While the heterozygote animals are viable, homozygote animals die at the 64-cell stage (Van Valen 1966) owing to a mitotic arrest (Magnuson et al. 1984).

Previous linkage studies have localized Os to the central portion of mouse Chromosome (Chr) 8 (reviewed by Ceci 1998; see also http://www. informatics. jax. org/bin/get mldp by marker? 12079). To further refine the linkage map position of the Os locus, we used linkage disequilibrium mapping with two extended pedigrees that were developed by selectively crossing the Os locus onto polymorphic backgrounds for over 20 years (http://www. informatics. jax. org/bin/fetch mlc? 12079)(Fig. 1). We hoped that by using genotype analysis of the Os/+ descendants from these pedigrees, ancestral alleles of only a few markers that were directly adjacent to the locus would be retained, whereas more proximal and distally located markers would be replaced with alleles from the newly introduced C57BL/6J and ROP strain backgrounds.