Distinct and redundant roles of the non-muscle myosin II isoforms and functional domains.
Distinct and redundant roles of the non-muscle myosin II isoforms and functional domains.
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DOI：
10.1042/bst0391131
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发表时间：
2011-10
影响因子：
3.9
通讯作者：
Adelstein RS
中科院分区：
文献类型：
--
作者：
Wang A;Ma X;Conti MA;Adelstein RS
我们认为，NM II(非肌肉肌球蛋白II)在体内的功能可以分为依赖于N端球状运动区的功能和依赖于运动活动但更依赖于C端结构域的功能。前者更多地依赖于NM II的动力学性质来转运肌动蛋白细丝，不太容易被不同的NM II亚型取代，而后者的体内功能涉及NM II与交联肌动蛋白细丝的结构特性，更容易被取代。根据这一假设，我们检验了NM II-A以及一种运动受损形式的NM II-B取代NM II-B并修复NM II-B耗竭小鼠大脑中的神经上皮细胞-细胞黏附缺陷和脑积水的能力。我们还检测了NM II-B以及嵌合形式的NM II(II-A头和II-B尾，反之亦然)在II-A消融小鼠的细胞-细胞黏附中替代NM II-A的能力。然而，我们也表明，某些功能，如发育中的大脑中的神经细胞迁移和小鼠胚胎和胎盘的血管形成，分别特别需要NM II-B和II-A。
We propose that the in vivo functions of NM II (non-muscle myosin II) can be divided between those that depend on the N-terminal globular motor domain and those less dependent on motor activity but more dependent on the C-terminal domain. The former, being more dependent on the kinetic properties of NM II to translocate actin filaments, are less amenable to substitution by different NM II isoforms, whereas the in vivo functions of the latter, which involve the structural properties of NM II to cross-link actin filaments, are more amenable to substitution. In light of this hypothesis, we examine the ability of NM II-A, as well as a motor-compromised form of NM II-B, to replace NM II-B and rescue neuroepithelial cell–cell adhesion defects and hydrocephalus in the brain of NM II-B-depleted mice. We also examine the ability of NM II-B as well as chimaeric forms of NM II (II-A head and II-B tail and vice versa) to substitute for NM II-A in cell–cell adhesions in II-A-ablated mice. However, we also show that certain functions, such as neuronal cell migration in the developing brain and vascularization of the mouse embryo and placenta, specifically require NM II-B and II-A respectively.