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Cerebral Cortex, Vol. 13, No. 6, 612-619, June 2003
© 2003 Oxford University Press

Pax6 Regulates Cell Adhesion during Cortical Development

David A. Tyas, Helen Pearson1, Penny Rashbass2 and David J. Price

Genes and Development Group, Biomedical Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, , 1 Nature Publishing Group, The Macmillan Building, 4 Crinan Street, London N1 9XW and , 2 Centre for Developmental Genetics, Department of Biomedical Science, University of Sheffield, Western Bank, Sheffield S10 2TN, UK

Address correspondence to Dr David Price, Genes and Development Group, Biomedical Sciences, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh EH8 9XD, UK. Email: dprice{at}ed.ac.uk.

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 Pax6Sey/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.


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