Disruption of Nectin-like 1 cell adhesion molecule leads to delayed axonal myelination in the CNS.
Disruption of Nectin-like 1 cell adhesion molecule leads to delayed axonal myelination in the CNS.
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DOI：
10.1523/jneurosci.2665-08.2008
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发表时间：
2008-11-26
期刊：
影响因子：
--
通讯作者：
Qiu M
中科院分区：
文献类型：
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作者：
Park J;Liu B;Chen T;Li H;Hu X;Gao J;Zhu Y;Zhu Q;Qiang B;Yuan J;Peng X;Qiu M
Nectin-like 1 （Necl-1）是一种神经特异性细胞粘附分子，在中枢神经系统和PNS中均有表达。先前的体外研究表明，在PNS中，Necl-1的表达对于轴突-胶质相互作用和髓鞘形成至关重要。为了研究Necl-1在发育中的神经系统轴突髓鞘形成中的体内作用，我们用LacZ报告基因替换轴突2-5，产生了Necl-1突变小鼠。表达研究表明，Necl-1仅在中枢神经系统神经元中表达。Necl-1的破坏导致视神经和脊髓轴突髓鞘形成的发育延迟，提示Necl-1在中枢神经系统髓鞘形成的初始轴突少突胶质细胞识别和粘附中起重要作用。
Nectin-like 1 (Necl-1) is a neural-specific cell adhesion molecule that is expressed in both the CNS and PNS. Previous in vitro studies suggested that Necl-1 expression is essential for the axon-glial interaction and myelin sheath formation in the PNS. To investigate the in vivo role of Necl-1 in axonal myelination of the developing nervous system, we generated the Necl-1 mutant mice by replacing axons 2–5 with the LacZ reporter gene. Expression studies revealed that Necl-1 is exclusively expressed by neurons in the CNS. Disruption of Necl-1 resulted in developmental delay of axonal myelination in the optic nerve and spinal cord, suggesting that Necl-1 plays an important role in the initial axon-oligodendrocyte recognition and adhesion in CNS myelination.