RESUMEN
We have previously shown that the rat fuzzy and Charles River 'hairless' mutations are defects in the same gene on rat Chr 1, and are likely orthologues of the frizzy mutation (fr) on mouse Chr 7. To test the hypothesis that these variants could result from defects in Fgfr2, we crossed fr/fr mice (from the inbred FS/EiJ strain) with mice that carry a recessive lethal mutation in Fgfr2. Mice inheriting both mutations were phenotypically normal, indicating that fr is not an allele of Fgfr2. To genetically map fr, we crossed these hybrid mice, or F(1) mice made by crossing FS/EiJ with the wild-type C57BL/6J or BALB/cBy strains, back to the FS/EiJ strain. The resulting 546 backcross progeny were typed for linked markers to position fr centromeric of Fgfr2, between D7Csu5 and D7Mit165; an interval that contains only 2.7 Mb and fewer than 70 genes. Further characterization of regional recombinants for sequence-level polymorphisms should allow sufficient refinement of fr's location to facilitate an eventual molecular assignment for this classical mutation.
