Marcus Jill, Dupree Jeffrey L, Popko Brian
UNC Neuroscience Center, University of North Carolina at Chapel Hill, 27599, USA.
J Cell Biol. 2002 Feb 4;156(3):567-77. doi: 10.1083/jcb.200111047.
We have analyzed mice that lack both the myelin-associated glycoprotein (MAG) and the myelin galactolipids, two glial components implicated in mediating axo-glial interactions during the myelination process. The single-mutant mice produce abnormal myelin containing similar ultrastructural abnormalities, suggesting that these molecules may play an overlapping role in myelin formation. Furthermore, the absence of the galactolipids results in a disruption in paranodal axo-glial interactions, and we show here that similar, albeit less severe, abnormalities exist in the developing MAG mutant. In the double-mutant mice, maintenance of axo-glial adhesion is significantly more affected than in the single mutants, supporting the overlapping function hypothesis. We also show that independently of MAG, galactolipids, and paranodal junctional components, immature nodes of Ranvier form normally, but rapidly destabilize in their absence. These data indicate that distinct molecular mechanisms are responsible for the formation and maintenance of axo-glial interactions.
我们分析了同时缺乏髓鞘相关糖蛋白（MAG）和髓鞘半乳糖脂的小鼠，这两种神经胶质成分在髓鞘形成过程中参与介导轴突与神经胶质的相互作用。单突变小鼠产生含有相似超微结构异常的异常髓鞘，这表明这些分子可能在髓鞘形成中发挥重叠作用。此外，半乳糖脂的缺失导致结旁轴突与神经胶质相互作用的破坏，并且我们在此表明，在发育中的MAG突变体中存在相似但不太严重的异常。在双突变小鼠中，轴突与神经胶质粘附的维持比单突变体受到的影响明显更大，这支持了重叠功能假说。我们还表明，独立于MAG、半乳糖脂和结旁连接成分，未成熟的郎飞结正常形成，但在它们缺失时会迅速不稳定。这些数据表明，不同的分子机制负责轴突与神经胶质相互作用的形成和维持。
