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Mapping the mouse dactylaplasia mutation, Dac, and a gene that controls its expression, mdac
K R Johnson1, P W Lane, P Ward-Bailey
1Jackson Laboratory, Bar Harbor, Maine 04609, USA.
Genomics
|September 20, 1995
Summary
Dactylaplasia (Dac) is a mouse limb malformation caused by gene interaction. This study maps the Dac and mdac genes, providing insights into inherited limb abnormalities and human ectrodactyly.
Area of Science:
- Genetics
- Developmental Biology
- Animal Models
Background:
- Dactylaplasia (Dac) is a semidominant inherited mouse limb malformation.
- It serves as a model for studying gene interactions and human ectrodactyly.
- Dac homozygotes typically die around birth on the SM/Ckc background.
Purpose of the Study:
- To map the Dactylaplasia (Dac) gene.
- To identify and map a second interacting gene, mdac.
- To understand the genetic basis of inherited limb malformations.
Main Methods:
- Backcross segregation analysis was used to map the Dac gene to chromosome 19.
- A linked marker distinguished Dac genotypes.
- Segregation analysis of recombinant inbred strains and backcross progeny mapped mdac to chromosome 13.
Main Results:
- The Dac gene was mapped to the distal end of chromosome 19.
- The interacting gene, mdac, was mapped to the middle of chromosome 13.
- Dac homozygotes are viable and show more severe limb malformations on the NZB/BINJ background.
Conclusions:
- The Dactylaplasia phenotype is dependent on the interaction between the Dac gene on chromosome 19 and the mdac gene on chromosome 13.
- This mouse model provides a system for studying gene interactions in vivo.
- The findings contribute to understanding the genetic etiology of limb malformations.