Myo10 is required for neurogenic cell adhesion and migration

Myo10 is required for neurogenic cell adhesion and migration
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Myo10 是神经源性细胞粘附和迁移所必需的

DOI:
10.1007/s11626-014-9845-z
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发表时间:
2015
影响因子:
2.1
通讯作者:
Zhu Xiaojuan
Zhu Xiaojuan
中科院分区:
生物学4区
文献类型:
--
作者:
Yu Huali;Lai Mingming;Guo Yuguang;Yuan Lin;Lan Yongsheng;Wang Xingzhi;Zhu Xiaojuan

文献摘要

相似文献

肌球蛋白 X (Myo10) 是肌球蛋白超家族的非传统成员,其特征是基于肌动蛋白的分子马达,在多种细胞运动事件中发挥着关键作用。我们课题组之前的研究发现Myo10影响发育中新皮质的神经元径向迁移,但其潜在机制仍不清楚。在这项研究中,我们发现,在转染大 T 抗原 (NLT) 的正常促性腺激素释放激素 (GnRH) 神经元细胞系中,内源性 Myo10 的敲低会导致细胞运动和定向受损。在伤口愈合测定中,通过高尔基复合体染色显示细胞极性,与对照相比,Myo10 敲低细胞的方向是随机的。此外,抑制 Myo10 的表达会降低细胞与基质的粘附能力。 N-钙粘蛋白是一种钙依赖性经典细胞粘附分子,可挽救细胞聚集体和胶原凝胶测定中因 Myo10 敲低而引起的迁移缺陷。这些结果表明,Myo10 是神经源性细胞通过 N-钙粘蛋白介导的细胞粘附迁移所必需的。
Myosin X (Myo10), an untraditional member of myosin superfamily, is characterized as an actin-based molecular motor, which plays a critical role in diverse cellular motile events. Previous research by our group has found that Myo10 influenced neuronal radial migration in developing neocortex, but the underlying mechanism is still largely unknown. In this study, we found that knockdown of endogenous Myo10 in a normal gonadotropin-releasing hormone (GnRH) neuronal cell line transfected with the large T antigen (NLT) induced the impairment of cell motility and orientation. In the wound healing assay, with the Golgi complex staining to display cell polarity, Myo10 knockdown cells were randomly oriented compared to the control. Furthermore, suppressing the expression of Myo10 decreased the ability of cell–matrix adhesion. N-cadherin, a calcium-dependent classical cell adhesion molecule, rescued the migration deficiency caused by Myo10 knockdown in cell aggregates and collagen gel assay. These results suggest that Myo10 is required for neurogenic cell migration through N-cadherin mediated cell adhesion.