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First published online 28 February 2007
doi: 10.1242/dev.02809

Development 134, 1311-1322 (2007)
Published by The Company of Biologists 2007
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Conditional activation of Pax6 in the developing cortex of transgenic mice causes progenitor apoptosis

Joachim Berger1, Silke Berger1, Tran Cong Tuoc1,2, Marcello D'Amelio3, Francesco Cecconi3, Jessica A. Gorski4, Kevin R. Jones4, Peter Gruss1 and Anastassia Stoykova1,2,*

1 Max Planck Institute for Biophysical Chemistry, D-37077 Göttingen, Germany.
2 DFG, Center of Molecular Physiology of the Brain (CMPB), Göttingen, Germany.
3 Dulbecco Telethon Institute at IRCCS Fondazione Santa Lucia, Rome, Italy.
4 University of Colorado, Boulder, Colorado, USA.

* Author for correspondence (e-mail: astoyko{at}gwdg.de)

Accepted 17 January 2007

During development, Pax6 is expressed in a rostrolateral-high to caudomedial-low gradient in the majority of the cortical radial glial progenitors and endows them with neurogenic properties. Using a Cre/loxP-based approach, we studied the effect of conditional activation of two Pax6 isoforms, Pax6 and Pax6-5a, on the corticogenesis of transgenic mice. We found that activation of either Pax6 or Pax6-5a inhibits progenitor proliferation in the developing cortex. Upon activation of transgenic Pax6, specific progenitor pools with distinct endogenous Pax6 expression levels at different developmental stages show defects in cell cycle progression and in the acquisition of apoptotic or neuronal cell fate. The results provide new evidence for the complex role of Pax6 in mammalian corticogenesis.

Key words: Corticogenesis, Cre/loxP, Overexpression, Pax6, Pax6-5a, Progenitor, Apoptosis, Mouse




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