P0 protein is required for and can induce formation of Schmidt-Lantermann incisures in myelin internodes
P0 protein is required for and can induce formation of Schmidt-Lantermann incisures in myelin internodes
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DOI：
10.1523/jneurosci.0771-08.2008
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发表时间：
2008-07-09
影响因子：
5.3
通讯作者：
Trapp, Bruce D.
中科院分区：
文献类型：
--
作者：
Yin, Xinghua;Kidd, Grahame J.;Trapp, Bruce D.
PNS和CNS的轴突被多层紧密压实的髓鞘膜包裹。一系列细胞质通道连接PNS的内外缘，但不连接CNS、髓鞘节间。这些施密特-兰登曼（S-L）切孔的膜含有髓鞘相关糖蛋白（MAG），但不含P-0或蛋白脂蛋白（PLP），即致密PNS （P-0）和CNS （PLP）髓鞘的结构蛋白。我们在这里发现，在MAG-null中存在切口，而在P-0-null的PNS节间不存在切口。为了检验P-0是否可能调控切缝形成，我们用CNS髓磷脂中的P-0代替PLP。P-0-CNS髓鞘节间形成S-L切口。此外，电镜检查65%的CNS切口包裹的轴质有局灶性的细胞器积聚，表明这些CNS切口破坏了轴突运输。这些数据支持了P-0蛋白是诱导S-L损伤所必需的假设，以及P-0诱导的中枢神经系统损伤可能对轴突功能有害的假设。
Axons in the PNS and CNS are ensheathed by multiple layers of tightly compacted myelin membranes. A series of cytoplasmic channels connect outer and inner margins of PNS, but not CNS, myelin internodes. Membranes of these Schmidt-Lantermann (S-L) incisures contain the myelin-associated glycoprotein (MAG) but not P-0 or proteolipid protein (PLP), the structural proteins of compact PNS (P-0) and CNS (PLP) myelin. We show here that incisures are present in MAG-null and absent from P-0-null PNS internodes. To test the possibility that P-0 regulates incisure formation, we replaced PLP with P-0 in CNS myelin. S-L incisures formed in P-0-CNS myelin internodes. Furthermore, axoplasm ensheathed by 65% of the CNS incisures examined by electron microscopy had focal accumulations of organelles, indicating that these CNS incisures disrupt axonal transport. These data support the hypotheses that P-0 protein is required for and can induce S-L incisures and that P-0-induced CNS incisures can be detrimental to axonal function.