Disruption of Nectin-Like 1 Cell Adhesion Molecule Leads to Delayed Axonal Myelination in the CNS

被引:47
作者
Park, Jinsil [3 ]
Liu, Ben [1 ,2 ]
Chen, Tao [1 ,2 ]
Li, Hong [3 ]
Hu, Xuemei [3 ]
Gao, Jing [1 ,2 ]
Zhu, Ying [3 ]
Zhu, Qiang [3 ]
Qiang, Boqin [1 ,2 ]
Yuan, Jiangang [1 ,2 ]
Peng, Xiaozhong [1 ,2 ]
Qiu, Mengsheng [3 ,4 ]
机构
[1] Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100005, Peoples R China
[2] Peking Union Med Coll, Beijing 100005, Peoples R China
[3] Univ Louisville, Sch Med, Dept Anat Sci & Neurobiol, Louisville, KY 40292 USA
[4] Tianjin Med Univ, Inst Urol Surg, Tianjin 300211, Peoples R China
基金
美国国家卫生研究院;
关键词
cell adhesion molecule; gene targeting; myelination; spinal cord; optic nerve; knock-out;
D O I
10.1523/JNEUROSCI.2665-08.2008
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:12815 / 12819
页数:5
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