Tang Chieh-Ju C, Fu Ru-Huei, Wu Kuo-Sheng, Hsu Wen-Bin, Tang Tang K
Institute of Biomedical Sciences, Taipei, Taiwan.
Nat Cell Biol. 2009 Jul;11(7):825-31. doi: 10.1038/ncb1889. Epub 2009 Jun 7.
Centriole duplication involves the growing of a procentriole (progeny centriole) next to the proximal end of each pre-existing centriole (parental centriole). The molecular mechanisms that regulate procentriole elongation remain obscure. We show here that expression of the centriolar protein CPAP (centrosomal P4.1-associated protein) is carefully regulated during the cell cycle, with the protein being degraded in late mitosis. Depletion of CPAP inhibited centrosome duplication, whereas excess CPAP induced the formation of elongated procentriole-like structures (PLSs), which contain stable microtubules and several centriolar proteins. Ultrastructural analysis revealed that these structures are similar to procentrioles with elongated microtubules. Overexpression of a CPAP mutant (CPAP-377EE) that does not bind to tubulin dimers significantly inhibited the formation of CPAP-induced PLSs. Together, these results suggest that CPAP is a new regulator of centriole length and its intrinsic tubulin-dimer binding activity is required for procentriole elongation.
中心粒复制涉及在每个已存在的中心粒（亲代中心粒）近端旁生长一个原中心粒（子代中心粒）。调节原中心粒伸长的分子机制仍不清楚。我们在此表明，中心粒蛋白CPAP（中心体P4.1相关蛋白）的表达在细胞周期中受到精确调控，该蛋白在有丝分裂后期被降解。CPAP缺失会抑制中心体复制，而过量的CPAP会诱导形成细长的原中心粒样结构（PLS），其包含稳定的微管和几种中心粒蛋白。超微结构分析表明，这些结构类似于具有细长微管的原中心粒。不与微管蛋白二聚体结合的CPAP突变体（CPAP-377EE）的过表达显著抑制了CPAP诱导的PLS的形成。总之，这些结果表明CPAP是中心粒长度的新调节因子，其内在的微管蛋白二聚体结合活性是原中心粒伸长所必需的。
