Further data on the slit‐lid mutant in mice and the effect of cortisone and doca on its development

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Abstract
The development of a mutant with eyelids open at birth that appeared in our laboratory was described previously (Stein et al., '67). It differed from similar mutants described in the literature and was called slit‐lids. Later Ricardo and Miller ('67) reported that complementarity tests between our mutant and another, called lid‐gap, indicated they were identical or allelic. They found that cortisone injected prenatally reduced the frequency of the lid‐gap phenotype (also reported by Watney and Miller, '64), but not of the slit‐lid mutants supplied by us. In our hands, however, cortisone did correct the defect in a large proportion of the slit‐lid progeny of injected pregnant females (Stein and Nichols, '68). Further experiments, reported here, confirmed our earlier results, and data from both series are combined in this paper. Injections of a mineralocorticoid, deoxycorticosterone, magnified the defects characterizing the untreated slit‐lid mutant. Histological data have been reviewed and supplemented for comparison with those of Harris and Fraser ('68) who reported no evidence in lid‐gap of the excessive vacuolation of the lens described by us in our mutant, but noted evidence of injurious adhesion of eyelids to cornea. In both respects the slit‐lid mutant appears to differ from lip‐gap.