Swaying is a mutant allele of the proto-oncogene Wnt-1

Mice homozygous for the recessive mutation swaying (SW) are characterized by ataxia and hypertonia, attributed to the malformation of anterior regions of the cerebellum. We show that SW is a deletion of a single base pair from the proto-oncogene Wnf-1. The deletion is predicted to cause premature termination of translation, eliminating the carboxy-terminal half of the Writ-1 protein. Histological examination shows that SW is phenotypically identical to a previously described writ-1 mutation introduced into mice by gene targeting.