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Nedd8类泛素蛋白修饰途径对细胞骨架的调控

Cytoskeletal regulation by the Nedd8 ubiquitin-like protein modification pathway.

作者信息

Kurz Thimo, Pintard Lionel, Willis John H, Hamill Danielle R, Gönczy Pierre, Peter Matthias, Bowerman Bruce

机构信息

Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.

出版信息

Science. 2002 Feb 15;295(5558):1294-8. doi: 10.1126/science.1067765.

Abstract

The Nedd8 ubiquitin-like protein modification pathway regulates cell-cycle progression. Our analysis of Nedd8 requirements during Caenorhabditis elegans embryogenesis indicates that the cytoskeleton is another target. Nedd8 conjugation negatively regulated contractility of the microfilament-rich cell cortex during pronuclear migration and again during cytokinesis. The Nedd8 pathway also was required after meiosis to negatively regulate katanin, a microtubule-severing complex, permitting the assembly of a large mitotic spindle. We propose that Nedd8-modified cullin, as part of an E3 ubiquitin ligase complex, targets katanin for degradation during the transition from meiosis to mitosis.

摘要

Nedd8类泛素蛋白修饰途径调控细胞周期进程。我们对线虫胚胎发育过程中Nedd8需求的分析表明,细胞骨架是另一个靶点。在原核迁移和胞质分裂过程中,Nedd8缀合均负向调控富含微丝的细胞皮层的收缩性。减数分裂后,Nedd8途径对于负向调控katanin(一种微管切断复合体)也是必需的,从而允许大型有丝分裂纺锤体的组装。我们提出,作为E3泛素连接酶复合体的一部分,Nedd8修饰的cullin在从减数分裂向有丝分裂转变过程中将katanin作为靶点进行降解。

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