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The Journal of Neuroscience, June 17, 2009, 29(24):7694-7705; doi:10.1523/JNEUROSCI.5537-08.2009

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Development/Plasticity/Repair
Regulation of Radial Glial Survival by Signals from the Meninges

Randor Radakovits,¹ Claudia S. Barros,¹ Richard Belvindrah,¹ Bruce Patton,² and Ulrich Müller¹

¹The Scripps Research Institute, Department of Cell Biology, Institute for Childhood and Neglected Disease, La Jolla, California 92037, and ²Oregon Health & Science University, Portland, Oregon 97239

Correspondence should be addressed to Ulrich Müller, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92073. Email: umueller{at}scripps.edu

Radial glial cells (RGCs) in the developing cerebral cortex are progenitors for neurons and glia, and their processes serve as guideposts for migrating neurons. So far, it has remained unclear whether RGC processes also control the function of RGCs more directly. Here, we show that RGC numbers and cortical size are reduced in mice lacking β1 integrins in RGCs. TUNEL stainings and time-lapse video recordings demonstrate that β1-deficient RGCs processes detach from the meningeal basement membrane (BM) followed by apoptotic death of RGCs. Apoptosis is also induced by surgical removal of the meninges. Finally, mice lacking the BM components laminin 2 and 4 show defects in the attachment of RGC processes at the meninges, a reduction in cortical size, and enhanced apoptosis of RGC cells. Our findings demonstrate that attachment of RGC processes at the meninges is important for RGC survival and the control of cortical size.

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Received Nov. 18, 2008; revised May 11, 2009; accepted May 13, 2009.

Correspondence should be addressed to Ulrich Müller, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92073. Email: umueller{at}scripps.edu

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