Abstract:
: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 Wnt-1. The deletion is predicted to cause premature termination of translation, eliminating the carboxy-terminal half of the Wnt-1 protein. Histological examination shows that sw is phenotypically identical to a previously described wnt-1 mutation introduced into mice by gene targeting. Although both mutations in Wnt-1 disrupt primarily the development of the anterior cerebellum, they also exhibit a variability in expressivity such that rostrally adjacent structures in the midbrain and caudally adjacent structures in the posterior cerebellum can also be affected.
journal_name
Celljournal_title
Cellauthors
Thomas KR,Musci TS,Neumann PE,Capecchi MRdoi
10.1016/0092-8674(91)90369-asubject
Has Abstractpub_date
1991-11-29 00:00:00pages
969-76issue
5eissn
0092-8674issn
1097-4172pii
0092-8674(91)90369-Ajournal_volume
67pub_type
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