Pax6 regulates cell adhesion during cortical development

Abstract

Pax6 is a member of an evolutionarily conserved family of transcription factors. It is developmentally regulated and is required for the normal embryonic development of the central nervous system, eye and pancreas. Pax6 mutations in the mouse result in the Small eye (Sey) phenotype. Heterozygous mice have eye defects and homozygotes die immediately after birth lacking eyes, nasal cavities and with severe brain abnormalities, including a malformed cerebral cortex. Recent work has established that there are changes in expression of cell adhesion molecules and these may underlie at least a part of the Pax6Sey/Sey phenotype. Here we used cell transplants and explant cultures to investigate the role of Pax6 in cell adhesion. Pax6Sey/Sey embryonic cortical cells transplanted into wild-type embryonic cortex were observed to segregate from wild-type cells and form dense clusters. Cells migrating from explants of PaxSey/Sey embryonic cortex clustered to a greater extent than cells migrating from wild-type controls. These new data support the hypothesis that Pax6 exerts a cell-autonomous effect on the adhesiveness of cortical cells.