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保守蛋白SZY-20对抗与Plk4相关的激酶ZYG-1以限制中心体大小。

The conserved protein SZY-20 opposes the Plk4-related kinase ZYG-1 to limit centrosome size.

作者信息

Song Mi Hye, Aravind L, Müller-Reichert Thomas, O'Connell Kevin F

机构信息

Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20894, USA.

出版信息

Dev Cell. 2008 Dec;15(6):901-12. doi: 10.1016/j.devcel.2008.09.018.

Abstract

Microtubules are organized by the centrosome, a dynamic organelle that exhibits changes in both size and number during the cell cycle. Here we show that SZY-20, a putative RNA-binding protein, plays a critical role in limiting centrosome size in C. elegans. SZY-20 localizes in part to centrosomes and in its absence centrosomes possess increased levels of centriolar and pericentriolar components including gamma-tubulin and the centriole duplication factors ZYG-1 and SPD-2. These enlarged centrosomes possess normal centrioles, nucleate more microtubules, and fail to properly direct a number of microtubule-dependent processes. Depletion of ZYG-1 restores normal centrosome size and function to szy-20 mutants, whereas loss of szy-20 suppresses the centrosome duplication defects in both zyg-1 and spd-2 mutants. Our results describe a pathway that determines centrosome size and implicate centriole duplication factors in this process.

摘要

微管由中心体组织而成,中心体是一种动态细胞器,在细胞周期中其大小和数量都会发生变化。我们在此表明,一种假定的RNA结合蛋白SZY-20在限制秀丽隐杆线虫中心体大小方面发挥着关键作用。SZY-20部分定位于中心体,在其缺失时,中心体中中心粒和中心粒周围成分(包括γ-微管蛋白以及中心粒复制因子ZYG-1和SPD-2)的水平会升高。这些增大的中心体拥有正常的中心粒,能形成更多微管,并且无法正确指导许多依赖微管的过程。ZYG-1的缺失可使szy-20突变体的中心体大小和功能恢复正常,而szy-20的缺失则可抑制zyg-1和spd-2突变体中的中心体复制缺陷。我们的研究结果描述了一条决定中心体大小的途径,并表明中心粒复制因子参与了这一过程。

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