Yue Tao, Xian Kendy, Hurlock Edward, Xin Mei, Kernie Steven G, Parada Luis F, Lu Q Richard
Center for Developmental Biology, Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
J Neurosci. 2006 Jan 25;26(4):1275-80. doi: 10.1523/JNEUROSCI.4717-05.2006.
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.
关于脊髓和后脑少突胶质细胞的解剖学来源的诸多争议已得到解决。然而，背侧和腹侧祖细胞对皮质髓鞘形成的相对贡献仍是一个争论的话题。为了评估背侧祖细胞对皮质髓鞘形成的贡献，我们在发育中的背侧端脑中敲除了碱性螺旋-环-螺旋转录因子Olig2。在Olig2敲除的皮质中，髓鞘形成在祖细胞阶段停滞。在这些条件下，腹侧来源的少突胶质细胞向背侧迁移到Olig2敲除区域，但不能完全弥补出生后阶段观察到的髓鞘形成缺陷。因此，Olig2功能的空间限制性敲除揭示了背侧祖细胞对皮质髓鞘形成的贡献，这一贡献比迄今所认识到的要大得多。
