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The Journal of Neuroscience, January 25, 2006, 26(4):1275-1280; doi:10.1523/JNEUROSCI.4717-05.2006

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Brief Communication
A Critical Role for Dorsal Progenitors in Cortical Myelination

Tao Yue,¹ Kendy Xian,¹ Edward Hurlock,¹ Mei Xin,^1,3 Steven G. Kernie,^1,2 Luis F. Parada,¹ and Q. Richard Lu^1,3

¹Center for Developmental Biology and Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, ²Department of Pediatrics, and ³Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390

Correspondence should be addressed to Dr. Q. Richard Lu, Center for Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Email: qrichard.lu{at}utsouthwestern.edu

Much controversy regarding the anatomical sources of oligodendrocytes in the spinal cord and hindbrain has been resolved. However, the relative contribution of dorsal and ventral progenitors to myelination of the cortex is still a subject of debate. To assess the contribution of dorsal progenitors to cortical myelination, we ablated the basic helix-loop-helix transcription factor Olig2 in the developing dorsal telencephalon. In Olig2-ablated cortices, myelination is arrested at the progenitor stage. Under these conditions, ventrally derived oligodendrocytes migrate dorsally into the Olig2-ablated territory but cannot fully compensate for myelination deficits observed at postnatal stages. Thus, spatially restricted ablation of Olig2 function unmasks a contribution of dorsal progenitors to cortical myelination that is much greater than hitherto appreciated.

Key words: cortex; knock-out mice; oligodendrocyte; bHLH transcription factor; Olig2; myelination

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Received Nov. 3, 2005; revised Dec. 11, 2005; accepted Dec. 18, 2005.

Correspondence should be addressed to Dr. Q. Richard Lu, Center for Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390. Email: qrichard.lu{at}utsouthwestern.edu

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