Mutations at the fused (Fu) locus on chromosome 17 of the mouse disrupt embryonic development by altering the organization of the neurectoderm. We have examined the interactions among several independent fused mutations, including a deletion of the locus, to define the nature of the mutant defects. Closely linked restriction fragment length polymorphisms made possible the unambiguous identification of genotype in all progeny. Tests with the deletion, as well as interactions among alleles, indicate that all three spontaneous mutations are "gain of function" defects. Comparisons of relative viabilities of the various mutant combinations rank them into a series of increasing severity and place constraints on possible modes of gene action.

Greenspan, R. J., & O’Brien, M. C. (1986). Genetic analysis of mutations at the fused locus in the mouse. Proceedings of the National Academy of Sciences, 83(12), 4413–4417.