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Oligodendrocyte Neurofascin Independently Regulates Both Myelin Targeting and Sheath Growth in the CNS.
Developmental Cell ( IF 10.7 ) Pub Date : 2019-11-21 , DOI: 10.1016/j.devcel.2019.10.016 Anna Klingseisen 1 , Ana-Maria Ristoiu 1 , Linde Kegel 1 , Diane L Sherman 1 , Maria Rubio-Brotons 1 , Rafael G Almeida 1 , Sigrid Koudelka 1 , Silvia K Benito-Kwiecinski 1 , Richard J Poole 2 , Peter J Brophy 1 , David A Lyons 1
Developmental Cell ( IF 10.7 ) Pub Date : 2019-11-21 , DOI: 10.1016/j.devcel.2019.10.016 Anna Klingseisen 1 , Ana-Maria Ristoiu 1 , Linde Kegel 1 , Diane L Sherman 1 , Maria Rubio-Brotons 1 , Rafael G Almeida 1 , Sigrid Koudelka 1 , Silvia K Benito-Kwiecinski 1 , Richard J Poole 2 , Peter J Brophy 1 , David A Lyons 1
Affiliation
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Selection of the correct targets for myelination and regulation of myelin sheath growth are essential for central nervous system (CNS) formation and function. Through a genetic screen in zebrafish and complementary analyses in mice, we find that loss of oligodendrocyte Neurofascin leads to mistargeting of myelin to cell bodies, without affecting targeting to axons. In addition, loss of Neurofascin reduces CNS myelination by impairing myelin sheath growth. Time-lapse imaging reveals that the distinct myelinating processes of individual oligodendrocytes can engage in target selection and sheath growth at the same time and that Neurofascin concomitantly regulates targeting and growth. Disruption to Caspr, the neuronal binding partner of oligodendrocyte Neurofascin, also impairs myelin sheath growth, likely reflecting its association in an adhesion complex at the axon-glial interface with Neurofascin. Caspr does not, however, affect myelin targeting, further indicating that Neurofascin independently regulates distinct aspects of CNS myelination by individual oligodendrocytes in vivo.
中文翻译：
少突胶质细胞神经成束蛋白独立调节中枢神经系统中的髓鞘靶向和鞘生长。
选择正确的髓鞘形成目标和调节髓鞘生长对于中枢神经系统 (CNS) 的形成和功能至关重要。通过斑马鱼的遗传筛选和小鼠的互补分析，我们发现少突胶质细胞神经肌成束蛋白的缺失导致髓鞘错误地靶向细胞体，而不影响靶向轴突。此外，Neurofascin 的损失通过损害髓鞘生长来减少 CNS 髓鞘形成。延时成像显示，单个少突胶质细胞的独特髓鞘形成过程可以同时参与靶标选择和鞘生长，并且神经肌成束蛋白同时调节靶向和生长。对少突胶质细胞神经束蛋白的神经元结合伙伴 Caspr 的破坏也会损害髓鞘生长，可能反映了它在轴突 - 神经胶质界面处的粘附复合物中与 Neurofascin 的关联。然而，Caspr 不影响髓鞘靶向，进一步表明 Neurofascin 在体内独立调节个体少突胶质细胞的 CNS 髓鞘形成的不同方面。
更新日期：2019-11-22
中文翻译：
少突胶质细胞神经成束蛋白独立调节中枢神经系统中的髓鞘靶向和鞘生长。
选择正确的髓鞘形成目标和调节髓鞘生长对于中枢神经系统 (CNS) 的形成和功能至关重要。通过斑马鱼的遗传筛选和小鼠的互补分析，我们发现少突胶质细胞神经肌成束蛋白的缺失导致髓鞘错误地靶向细胞体，而不影响靶向轴突。此外，Neurofascin 的损失通过损害髓鞘生长来减少 CNS 髓鞘形成。延时成像显示，单个少突胶质细胞的独特髓鞘形成过程可以同时参与靶标选择和鞘生长，并且神经肌成束蛋白同时调节靶向和生长。对少突胶质细胞神经束蛋白的神经元结合伙伴 Caspr 的破坏也会损害髓鞘生长，可能反映了它在轴突 - 神经胶质界面处的粘附复合物中与 Neurofascin 的关联。然而，Caspr 不影响髓鞘靶向，进一步表明 Neurofascin 在体内独立调节个体少突胶质细胞的 CNS 髓鞘形成的不同方面。
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