Dactylaplasia in mice a two-locus model for development anomalies.

Authors

C K. Chai

Document Type

Article

Publication Date

1981

Keywords

Crosses-Genetic, Evolution, Extremities: ab, Female, Genes-Dominant, Male, Mice, Mice-Inbred-Strains: ge, Models-Genetic, Nomenclature, SUPPORT-U-S-GOVT-P-H-S

First Page

234

Last Page

237

JAX Location

40,912

JAX Source

J-Hered. 1981 Jul-Aug; 72(4):234-7.

Grant

AG02122

Abstract

Dactylaplasia, characterized by the absence of phalangeal bones in the middle digits of each foot, resulted from a mutation that occurred in the SM7B/SM inbred strain of mice. Breeding tests revealed the mutant gene is an autosomal dominant that is homozygous lethal. Further investigation by outcrossing with a number of inbred strains showed that the manifestation of the mutant gene is controlled by another locus. At this locus are found two alleles: one, a dominant inhibiting dactylaplasia gene expression; the other, a recessive allowing the expression of the mutant gene. In each of the tested inbred strains, one or the other allele is present at this locus. We propose Dac as a symbol for the mutant gene, and mdac for the locus controlling the Dac expression. Mouse dactylaphasia closely resembles split hand/foot in man and in monkeys in gross morphology and mode of inheritance. The significance of the present findings explainable by a two-locus model is discussed relative to irregular mode of inheritance of certain other congenital defects, and also relative to the maintenance of genetic loads in populations.

Recommended Citation

Chai CK. Dactylaplasia in mice a two-locus model for development anomalies. J-Hered. 1981 Jul-Aug; 72(4):234-7.