Department of Cell and Molecular Biology, Queensland Institute of Medical Research, Brisbane, QLD, Australia.
Cell Cycle. 2013 Mar 15;12(6):899-906. doi: 10.4161/cc.23879. Epub 2013 Feb 26.
The amount of pericentriolar matrix at the centrosome is tightly linked to both microtubule nucleation and centriole duplication, although the exact mechanism by which pericentriolar matrix levels are regulated is unclear. Here we show that Centrobin, a centrosomal protein, is involved in regulating these levels. Interphase microtubule arrays in Centrobin-depleted cells are more focused around the centrosome and are less stable than the arrays in control cells. Centrobin-depleted cells initiate microtubule nucleation more rapidly than control cells and exhibit an increase in the number of growing microtubule ends emanating from the centrosome, while the parameters of microtubule plus end dynamics around the centrosome are not significantly altered. Finally, we show that Centrobin depletion results in the increased recruitment of pericentriolar matrix proteins to the centrosome, including γ-tubulin, AKAP450, Kendrin and PCM-1. We propose that Centrobin might regulate microtubule nucleation and organization by controlling the amount of pericentriolar matrix.
中心体周围基质的含量与微管的起始和中心体的复制紧密相关，尽管目前尚不清楚调节中心体周围基质水平的确切机制。在这里，我们发现中心体蛋白Centrobin参与了这一过程的调节。在 Centrobin 敲低的细胞中，有丝分裂期微管围绕中心体更加集中，且稳定性较对照组细胞差。Centrobin 敲低的细胞起始微管起始的速度快于对照组细胞，并且从中心体延伸出的生长微管末端数量增加，而微管正端动力学参数在中心体周围并没有显著改变。最后，我们发现 Centrobin 敲低导致中心体周围基质蛋白（包括γ-微管蛋白、AKAP450、Kendrin 和 PCM-1）募集增加。我们推测，Centrobin 可能通过控制中心体周围基质的含量来调节微管的起始和组织。
