Coronin 1C is an established modulator of actin cytoskeleton dynamics. It has been shown to be involved in protrusion formation, cell migration and invasion. Here, we report the generation of primary fibroblasts from coronin 1C knock-out mice in order to investigate the impact of the loss of coronin 1C on cellular structural organisation. We demonstrate that the lack of coronin 1C not only affects the actin system, but also the microtubule and the vimentin intermediate filament networks. In particular, we show that the knock-out cells exhibit a reduced proliferation rate, impaired cell migration and protrusion formation as well as an aberrant subcellular localisation and function of mitochondria. Moreover, we demonstrate that coronin 1C specifically interacts with the non-α-helical amino-terminal domain ("head") of vimentin. Our data suggest that coronin 1C acts as a cytoskeletal integrator of actin filaments, microtubules and intermediate filaments.

中文翻译：

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不含Coronin 1C的原代小鼠成纤维细胞在肌动蛋白丝，微管和中间丝的方向上表现出强健的重排。

Coronin 1C是肌动蛋白细胞骨架动力学的既定调节剂。已经显示出它参与突起形成，细胞迁移和侵袭。在这里，我们报道了从冠状蛋白1C敲除小鼠中生成初级成纤维细胞的目的，以研究冠状蛋白1C的丢失对细胞结构组织的影响。我们证明冠蛋白1C的缺乏不仅影响肌动蛋白系统，而且影响微管和波形蛋白中间丝网络。特别地，我们显示出敲除细胞表现出降低的增殖速率，受损的细胞迁移和突起形成以及异常的亚细胞定位和线粒体功能。而且，我们证明冠蛋白1C与波形蛋白的非α-螺旋氨基末端结构域（“头部”）特异性相互作用。