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An Integrated Approach for Microprotein Identification and Sequence Analysis
Published on: July 12, 2022
The mouse frizzy mutation (fr) maps between D7Csu5 and D7Mit165
Emily L Paul1, Romina Badal, David S Thompson
1Biomolecular Sciences, Central Connecticut State University, New Britain, Connecticut, USA.
Experimental Dermatology
|January 8, 2008
Summary
The mouse frizzy (fr) mutation is not caused by a defect in Fgfr2. Genetic mapping positioned fr centromeric to Fgfr2, narrowing the search for this gene.
Area of Science:
- Genetics
- Developmental Biology
Background:
- The rat fuzzy and Charles River 'hairless' mutations are defects in the same gene on rat chromosome 1.
- These mutations are likely orthologues of the mouse frizzy (fr) mutation on mouse chromosome 7.
Purpose of the Study:
- To test the hypothesis that the frizzy (fr) mutation results from defects in the Fibroblast Growth Factor Receptor 2 (Fgfr2) gene.
- To genetically map the location of the frizzy (fr) mutation.
Main Methods:
- Crossed homozygous frizzy (fr/fr) mice with mice carrying a recessive lethal mutation in Fgfr2.
- Performed genetic mapping by crossing F(1) hybrid mice back to the homozygous frizzy strain.
- Typed 546 backcross progeny for linked markers.
Main Results:
- Mice inheriting both the fr and Fgfr2 mutations were phenotypically normal, indicating fr is not an allele of Fgfr2.
- Genetic mapping positioned the fr mutation centromeric to Fgfr2, between markers D7Csu5 and D7Mit165.
- This interval spans 2.7 Mb and contains fewer than 70 genes.
Conclusions:
- The frizzy (fr) mutation is distinct from Fgfr2.
- Further characterization of this refined interval will facilitate the molecular identification of the gene responsible for the frizzy mutation.
