Kinoshita M, Kumar S, Mizoguchi A, Ide C, Kinoshita A, Haraguchi T, Hiraoka Y, Noda M
Department of Molecular Oncology, Graduate School of Medicine, Kyoto University, Japan.
Genes Dev. 1997 Jun 15;11(12):1535-47. doi: 10.1101/gad.11.12.1535.
The mouse Nedd5 gene encodes a 41.5-kD GTPase similar to the Saccharomyces and Drosophila septins essential for cytokinesis. Nedd5 accumulates near the contractile ring from anaphase through telophase, and finally condenses into the midbody. Microinjection of anti-Nedd5 antibody interferes with cytokinesis, giving rise to binucleated cells. In interphase and postmitotic cells, Nedd5 localizes to fibrous or granular structures depending on the growth state of the cell. The Nedd5-containing fibers are disrupted by microinjection of GTPgammaS and by Nedd5 mutants lacking GTP-binding activity, implying that GTP hydrolysis is required for its assembly. The Nedd5-containing fibers also appear to physically contact actin bundles and focal adhesion complexes and are disrupted by cytochalasin D, C3 exoenzyme, and serum starvation, suggesting a functional interaction with the actin-based cytoskeletal systems in interphase cells.
小鼠Nedd5基因编码一种41.5-kD的GTP酶，类似于酿酒酵母和果蝇中对胞质分裂至关重要的septins。Nedd5从后期到末期在收缩环附近积累，最终浓缩成中体。显微注射抗Nedd5抗体干扰胞质分裂，产生双核细胞。在间期和有丝分裂后细胞中，Nedd5根据细胞的生长状态定位于纤维状或颗粒状结构。含Nedd5的纤维被显微注射GTPγS以及缺乏GTP结合活性的Nedd5突变体破坏，这意味着GTP水解是其组装所必需的。含Nedd5的纤维似乎也与肌动蛋白束和粘着斑复合物发生物理接触，并被细胞松弛素D、C3外切酶和血清饥饿破坏，表明在间期细胞中与基于肌动蛋白的细胞骨架系统存在功能相互作用。
