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Ermin is a p116RIP -interacting protein promoting oligodendroglial differentiation and myelin maintenance.
Glia ( IF 5.4 ) Pub Date : 2020-06-12 , DOI: 10.1002/glia.23838 Shan Wang 1 , Tao Wang 2 , Tao Liu 3 , Rou-Gang Xie 4 , Xiang-Hui Zhao 4 , Lei Wang 1 , Qian Yang 2 , Lin-Tao Jia 1 , Jing Han 3
Glia ( IF 5.4 ) Pub Date : 2020-06-12 , DOI: 10.1002/glia.23838 Shan Wang 1 , Tao Wang 2 , Tao Liu 3 , Rou-Gang Xie 4 , Xiang-Hui Zhao 4 , Lei Wang 1 , Qian Yang 2 , Lin-Tao Jia 1 , Jing Han 3
Affiliation
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Myelin sheaths, which insulate the axons and ensure saltatory conduction of the nerve impulse, are generated and maintained via largely uncharacterized mechanisms. Ermin is an oligodendrocyte‐specific protein associated with the cytoskeleton, but how it regulates cytoskeletal remodeling during oligodendrocyte differentiation and its role in myelin maintenance are not clear. To address this, we generated mice constitutively deficient for Ermn, the Ermin‐coding gene. We found that aged Ermn‐knockout mice exhibit an aberrant myelin architecture, with splitting of myelin layers, peeling of the myelin sheath from axons, and breakdown of myelinated fibers. As a result, these mice had remarkably impaired motor coordination. Ermn knockout also accelerated cuprizone‐induced demyelination and exacerbated the associated movement disorders. Ermin was found to contribute to oligodendrocyte morphogenesis by associating with the myosin phosphatase Rho interacting protein (Mprip/p116RIP) and inactivating RhoA, a GTPase that controls cytoskeletal rearrangement in differentiating cells. These findings provide novel insights into the mechanisms regulating oligodendroglial differentiation, the maintenance of the myelin sheaths, and remyelination.
中文翻译：
Ermin 是一种 p116RIP 相互作用蛋白，可促进少突胶质细胞分化和髓鞘维持。
髓鞘使轴突绝缘并确保神经冲动的跳跃式传导，它是通过很大程度上未表征的机制产生和维持的。Ermin 是一种与细胞骨架相关的少突胶质细胞特异性蛋白，但它在少突胶质细胞分化过程中如何调节细胞骨架重塑及其在髓鞘维持中的作用尚不清楚。为了解决这个问题，我们生成了 Ermin 编码基因Ermn组成性缺陷的小鼠。我们发现年老的Ermn基因敲除小鼠表现出异常的髓鞘结构，髓鞘层分裂，髓鞘从轴突上剥落，髓鞘纤维断裂。结果，这些小鼠的运动协调能力明显受损。恩恩敲除还加速了铜宗诱导的脱髓鞘并加剧了相关的运动障碍。Ermin 被发现通过与肌球蛋白磷酸酶 Rho 相互作用蛋白 (Mprip/p116 RIP ) 相关联并灭活 RhoA（一种控制分化细胞中细胞骨架重排的 GTPase）来促进少突胶质细胞形态发生。这些发现为调节少突胶质细胞分化、髓鞘的维持和髓鞘再生的机制提供了新的见解。
更新日期：2020-06-12
中文翻译：
Ermin 是一种 p116RIP 相互作用蛋白，可促进少突胶质细胞分化和髓鞘维持。
髓鞘使轴突绝缘并确保神经冲动的跳跃式传导，它是通过很大程度上未表征的机制产生和维持的。Ermin 是一种与细胞骨架相关的少突胶质细胞特异性蛋白，但它在少突胶质细胞分化过程中如何调节细胞骨架重塑及其在髓鞘维持中的作用尚不清楚。为了解决这个问题，我们生成了 Ermin 编码基因Ermn组成性缺陷的小鼠。我们发现年老的Ermn基因敲除小鼠表现出异常的髓鞘结构，髓鞘层分裂，髓鞘从轴突上剥落，髓鞘纤维断裂。结果，这些小鼠的运动协调能力明显受损。恩恩敲除还加速了铜宗诱导的脱髓鞘并加剧了相关的运动障碍。Ermin 被发现通过与肌球蛋白磷酸酶 Rho 相互作用蛋白 (Mprip/p116 RIP ) 相关联并灭活 RhoA（一种控制分化细胞中细胞骨架重排的 GTPase）来促进少突胶质细胞形态发生。这些发现为调节少突胶质细胞分化、髓鞘的维持和髓鞘再生的机制提供了新的见解。
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