Studies on an Anophthalmic Strain of Mice. IV. a Second Major Gene for Anophthalmia.

NHERITANCE of eyelessness in mice has been discussed in a previous I paper (CHASE 194zb) in which the method of analysis was the crossing of the inbred eyeless strain with other strains. The present study considers another method suggested a t that time, involving a control of modifiers. This was made possible by a reverse mutation toward normal eyes in the eyeless strain. From the mutant individual two sublines have been developed, one with 98 percent anophthalmic mice, the other with 96 percent normals (preliminary report CHASE 1942a). The fundamental phenomenon in the embryology of the eyeless strain is the inhibition of the growth of the optic vesicle a t ten days or earlier, just after the normal formation of the vesicle (CHASE and CHASE 1941). Because of variations in the degree of inhibition, ten percent of the original strain have ‘%mall” or “medium” eyes as observed a t birth or postmortem. From the previous study (CHASE 1942b) of crosses of anophthalmic strain B with strain C57 Black and with strain K, one major factor difference, ey recessive for eyelessness, was deduced. From results of crosses with strains L and H, two hypotheses were suggested. In one hypothesis two major factors were present with one dominant sufficient for normal eyes (double recessive necessary for eyelessness) and strong minus modifiers from strain B. I n the other hypothesis there was one major factor with dominance of normal eyes and strong plus modifiers from L and H The present paper will give additional evidence that the original anophthalmic strain is homozygous for one major factor, ey ey, and will present data to show that it is homozygous for another major factor for anophthalmi’a, present also in C57 Black but not in L and H.