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The Journal of Neuroscience, July 19, 2006, 26(29):7665-7673; doi:10.1523/JNEUROSCI.0444-06.2006

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Development/Plasticity/Repair
1-Integrin Signaling Mediates Premyelinating Oligodendrocyte Survival But Is Not Required for CNS Myelination and Remyelination

Yves Benninger,¹ Holly Colognato,² Tina Thurnherr,¹ Robin J. M. Franklin,³ Dino P. Leone,¹ Suzana Atanasoski,¹ Klaus-Armin Nave,⁴ Charles ffrench-Constant,² Ueli Suter,¹ and João B. Relvas¹

¹Institute for Cell Biology, Department of Biology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland, ²Departments of Medical Genetics and Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom, ³Cambridge Centre for Brain Repair, and Neuroregeneration Laboratory, Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, United Kingdom, and ⁴Department of Neurogenetics, Max Planck Institute of Experimental Medicine, 37075 Goettingen, Germany

Correspondence should be addressed to either João B. Relvas or Ueli Suter, Institute for Cell Biology, Department of Biology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland. Email: joao.relvas{at}cell.biol.ethz.ch or Email: usuter{at}cell.biol.ethz.ch

Previous reports, including transplantation experiments using dominant-negative inhibition of 1-integrin signaling in oligodendrocyte progenitor cells, suggested that 1-integrin signaling is required for myelination. Here, we test this hypothesis using conditional ablation of the 1-integrin gene in oligodendroglial cells during the development of the CNS. This approach allowed us to study oligodendroglial 1-integrin signaling in the physiological environment of the CNS, circumventing the potential drawbacks of a dominant-negative approach. We found that 1-integrin signaling has a much more limited role than previously expected. Although it was involved in stage-specific oligodendrocyte cell survival, 1-integrin signaling was not required for axon ensheathment and myelination per se. We also found that, in the spinal cord, remyelination occurred normally in the absence of 1-integrin. We conclude that, although 1-integrin may still contribute to other aspects of oligodendrocyte biology, it is not essential for myelination and remyelination in the CNS.

Key words: integrins; oligodendrocytes; survival; myelin; remyelination; CNS

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Received Aug. 30, 2005; revised May 29, 2006; accepted May 31, 2006.

Correspondence should be addressed to either João B. Relvas or Ueli Suter, Institute for Cell Biology, Department of Biology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland. Email: joao.relvas{at}cell.biol.ethz.ch or Email: usuter{at}cell.biol.ethz.ch

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