A spontaneous occurrence of polydactyly in mice failed to comply with any acceptable segregation ratio, but its genetic basis was established by its rapid response to selection. Both the incidence and the severity of abnormality increased. Initially manifested as one extra digit on one hind foot only, the polydactyly spread to both hind feet, and the number of supernumerary digits rose. Subsequently, the fore feet became affected as well, and in those cases, the hind legs became deformed in a manner reminiscent of the luxate mutant. The genetic interpretation of the data was compatible with a model of liability to the abnormality based on a continuously distributed underlying variable, with two thresholds, one corresponding to hind foot polydactyly alone and a higher threshold which, when exceeded, made the mice polydactylous on the fore feet as well. Further analyses indicated that the threshold for the hind foot condition was in fact a cluster of thresholds, corresponding to increasing digit numbers. The data revealed complex interactions between systemic and local influences on digit number, with implications for the gene control of limb development.