title: The lidgap defect in mice: update and hypotheses.
abstract: The open eye defect in the mouse can result from the action of mutant genes or of teratogens. Among the genetic forms, the lidgap series poses a particular challenge. The lidgap defect appears to be a complex genetic trait and may serve as a model for the genetic analysis of other genetically complex morphological defects in mammals. Extensive breeding data, together with data on the response of the trait to in utero treatment with cortisone, have been analyzed. The results lead us to propose a model involving a single major locus with a series of alleles of graded strength, hypomorphs. The ranking is lg greater than lgstn = lgSt greater than lgM1. The lg/lg genotype alone can be sufficient to produce the lidgap trait, but the "weaker" alleles require a second or even third locus acting in the same pathway. In addition, there is evidence that a recessive suppressor locus is present in the system. These hypotheses are testable and some experiments to develop them further are discussed.
mesh_terms: D000483:Alleles; D000818:Animals; D003348:Cortisone / Q000494:pharmacology; D003433:Crosses, Genetic; D005143:Eyelids / Q000002:abnormalities* / Q000187:drug effects; D005260:Female; D005808:Genes, Recessive; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D008957:Models, Genetic; D013489:Suppression, Genetic
chemical_list: D003348:Cortisone