Lethal Action in the Short-Tailed Mutation in the House Mouse

Abstract

Three dominant factors in which the homozygous mutant form does not exist are known in mice, viz., yellow coat color (A^y), black-eyed white (W), and brachyury. In all of these cases crosses inter se yield an F₁ of 2 mutants to one normal. Crosses to normals give a 1:1 ratio. These facts are explained by the supposition that the presence of 2 factors for the mutant character has a lethal action at some period during the development. Little and Castle, 1 following Cuénot, first advanced this hypothesis as to yellow mice. Subsequent investigation seems to show that the action takes place very early in embryogeny. Aberle 2 traced the lethal action in black-eyed white mice to an anemic condition. Here the homozygous anemics may survive to birth and live a short time afterwards. The breeding experiments of N. Dobrovalskia-Zavadskia 3 have indicated that a lethal action probably accompanies dominant short-tailedness (brachyury). The length of the tail varies. A few are indistinguishable from normal except for a slight bluntness. Others have no external tail. The latter have a varying number of malformed caudals and a derangement of the sacral and lumbar vertebrae. One or more rigid bends caused by an ankylosis of vertebrae often accompany the shortening. A paralysis of the posterior limbs is occasionally encountered. It seems probable that this latter condition is the result of abnormalities in the sacral and lumbar vertebrae.

My object was to discover the stage at which the lethal action of this gene occurs and to describe its effect on development. In matings of brachyurie X brachyurie embryos are found at the last of the eighth day, while still in the stage of the primary flexure, which show definite abnormalities.