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First published online 8 June 2005
doi: 10.1242/dev.01891

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PTEN deletion in Bergmann glia leads to premature differentiation and affects laminar organization

¹ Department of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, USA
² Molecular Biology Institute, University of California, Los Angeles, CA 90095, USA
³ Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA
⁴ Department of Pathobiological Sciences and Waisman Center, University of Wisconsin, Madison, WI 53705, USA
⁵ Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA 90095, USA

^* Author for correspondence (e-mail: xliu{at}mednet.ucla.edu)

Accepted 5 May 2005

Development of the central nervous system is controlled by both intrinsic and extrinsic signals that guide neuronal migration to form laminae. Although defects in neuronal mobility have been well documented as a mechanism for abnormal laminar formation, the role of radial glia, which provide the environmental cues, in modulating neuronal migration is less clear. We provide evidence that loss of PTEN in Bergmann glia leads to premature differentiation of this crucial cell population and subsequently to extensive layering defects. Accordingly, severe granule neuron migration defects and abnormal laminar formation are observed. These results uncover an unexpected role for PTEN in regulating Bergmann glia differentiation, as well as the importance of time-dependent Bergmann glia differentiation during cerebellar development.

Key words: PTEN, Bergmann glia, Cerebellar development, Mouse

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