RT Journal Article
SR Electronic
T1 Disruption of <em>Nectin-Like 1</em> Cell Adhesion Molecule Leads to Delayed Axonal Myelination in the CNS
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 12815
OP 12819
DO 10.1523/JNEUROSCI.2665-08.2008
VO 28
IS 48
A1 Jinsil Park
A1 Ben Liu
A1 Tao Chen
A1 Hong Li
A1 Xuemei Hu
A1 Jing Gao
A1 Ying Zhu
A1 Qiang Zhu
A1 Boqin Qiang
A1 Jiangang Yuan
A1 Xiaozhong Peng
A1 Mengsheng Qiu
YR 2008
UL http://www.jneurosci.org/content/28/48/12815.abstract
AB 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.