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The Journal of Neuroscience, August 16, 2006, 26(33):8417-8427; doi:10.1523/JNEUROSCI.1578-06.2006

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Development/Plasticity/Repair
TGF Type II Receptor Signaling Controls Schwann Cell Death and Proliferation in Developing Nerves

Maurizio D’Antonio,^1 * Anna Droggiti,^1 * M. Laura Feltri,³ Jürgen Roes,² Lawrence Wrabetz,³ Rhona Mirsky,¹ and Kristján R. Jessen¹

Departments of ¹Anatomy and Developmental Biology and ²Immunology and Molecular Pathology, University College London, London WC1E 6BT, United Kingdom, and ³Department of Biological and Technological Research, San Raffaele Scientific Institute, 20132 Milano, Italy

Correspondence should be addressed to Dr. Jessen at the above address. Email: k.jessen{at}ucl.ac.uk

During development, Schwann cell numbers are precisely adjusted to match the number of axons. It is essentially unknown which growth factors or receptors carry out this important control in vivo. Here, we tested whether the type II transforming growth factor (TGF) receptor has a role in this process. We generated a conditional knock-out mouse in which the type II TGF receptor is specifically ablated only in Schwann cells. Inactivation of the receptor, evident at least from embryonic day 18, resulted in suppressed Schwann cell death in normally developing and injured nerves. Notably, the mutants also showed a strong reduction in Schwann cell proliferation. Consequently, Schwann cell numbers in wild-type and mutant nerves remained similar. Lack of TGF signaling did not appear to affect other processes in which TGF had been implicated previously, including myelination and response of adult nerves to injury. This is the first in vivo evidence for a growth factor receptor involved in promoting Schwann cell division during development and the first genetic evidence for a receptor that controls normal developmental Schwann cell death.

Key words: Schwann cell; proliferation; death; TGF; neuregulin; CRE recombinase

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Received April 12, 2006; revised June 13, 2006; accepted June 15, 2006.

Correspondence should be addressed to Dr. Jessen at the above address. Email: k.jessen{at}ucl.ac.uk

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