Some observations on the microphthalmia gene in the mouse
The gene for microphthalmia in the mouse described by Hertwig shows a greatly reduced secondary bone absorption throughout its skeleton in the homozygous condition. It closely resembles in this respect, and in the reduction of pigmentation, the grey-lethal mouse in which the failure of bone absorption is complete. The two genes are, however, not allelomorphic to each other; it remains uncertain whether they are carried in different chromosomes.
In heterozygous condition, the gene for microphthalmia dilutes the choroidal pigmentation of the eye. The separability of the heterozygotes from +/+ normals is practically complete in the eight genotypes resulting from the combination of the genesA v. a, B v. b, andD v. d.
Depending on the genetic background in which it finds itself, the gene for microphthalmia in heterozygous condition may act as a spotting gene. Spotting results in the presence of certain ‘specific modifiers’ which do not produce spotting by themselves. In addition, themi gene also enhances the effect of certain minor genes which produce tail spotting in their own right. The spotting starts on the tail tip and in more marked cases spreads to the belly and/or the forehead; it always keeps in close proximity to the midline of the body. In the absence of these genes, +/mi shows no spotting whatever; the gene is thus not a spotting gene in its own right.
The bearing of the case on certain questions of pleiotropic gene action, on the distinction between ‘colour’ and ‘spotting’ genes, and between ‘main’ and ‘modifying’ genes is briefly discussed.
Volume 100, 2021
Continuous Article Publishing mode
Click here for Editorial Note on CAP Mode