Aberrant fragment of Dab1 protein is present in yotari mouse

• A mutant mouse yotari expresses an aberrant Dab1 fragment p64/60.
• Expression of p64/60 is higher in embryonic stages than in postnatal ones.
• p64/60 is not phosphorylated and localizes mainly to the nucleus.
• Use of yotari as a Dab1-null mouse should be done so with caution.

The Reelin–Dab1 pathway plays important roles in the development of central nervous system. In the autosomal recessive mutant mouse yotari, there is a replacement of a part of Dab1 gene with a long interspersed nuclear element fragment, and it was previously suggested that no protein derived from this gene was present. We here show that an aberrant fragment of Dab1 protein (p64/60) is present in the brain of yotari mouse. The amount of p64/60 is relatively abundant in the embryonic stages and decreased in the postnatal ones. Unlike wild-type Dab1 protein, p64/60 is not phosphorylated by Fyn kinase and localizes considerably to the nucleus. These data suggested that some phenotypes of yotari may be attributable to the presence of p64/60. It also raises a caveat that a tissue from yotari is not a perfect control for immunostaining of Dab1 protein.