Max Planck Institute for Molecular Genetics, Department of Vertebrate Genomics, Berlin, Germany.
Mol Cell Biol. 2012 Sep;32(17):3554-69. doi: 10.1128/MCB.00814-12. Epub 2012 Jul 2.
Phosphorylation is one of the key mechanisms that regulate centrosome biogenesis, spindle assembly, and cell cycle progression. However, little is known about centrosome-specific phosphorylation sites and their functional relevance. Here, we identified phosphoproteins of intact Drosophila melanogaster centrosomes and found previously unknown phosphorylation sites in known and unexpected centrosomal components. We functionally characterized phosphoproteins and integrated them into regulatory signaling networks with the 3 important mitotic kinases, cdc2, polo, and aur, as well as the kinase CkIIβ. Using a combinatorial RNA interference (RNAi) strategy, we demonstrated novel functions for P granule, nuclear envelope (NE), and nuclear proteins in centrosome duplication, maturation, and separation. Peptide microarrays confirmed phosphorylation of identified residues by centrosome-associated kinases. For a subset of phosphoproteins, we identified previously unknown centrosome and/or spindle localization via expression of tagged fusion proteins in Drosophila SL2 cells. Among those was otefin (Ote), an NE protein that we found to localize to centrosomes. Furthermore, we provide evidence that it is phosphorylated in vitro at threonine 63 (T63) through Aurora-A kinase. We propose that phosphorylation of this site plays a dual role in controlling mitotic exit when phosphorylated while dephosphorylation promotes G(2)/M transition in Drosophila SL2 cells.
磷酸化是调节中心体生物发生、纺锤体组装和细胞周期进程的关键机制之一。然而,对于中心体特异性磷酸化位点及其功能相关性知之甚少。在这里,我们鉴定了完整的黑腹果蝇中心体的磷酸蛋白,并在已知和意外的中心体成分中发现了以前未知的磷酸化位点。我们对磷酸蛋白进行了功能表征,并将其与 3 种重要的有丝分裂激酶(cdc2、polo 和 aur)以及激酶 CkIIβ整合到调控信号网络中。通过组合 RNA 干扰(RNAi)策略,我们证明了 P 颗粒、核膜(NE)和核蛋白在中心体复制、成熟和分离中的新功能。肽微阵列通过在果蝇 SL2 细胞中表达标记融合蛋白证实了鉴定的残基被中心体相关激酶磷酸化。对于一组磷酸蛋白,我们通过在果蝇 SL2 细胞中表达标记融合蛋白鉴定了以前未知的中心体和/或纺锤体定位。其中包括 otefin(Ote),一种我们发现定位于中心体的 NE 蛋白。此外,我们提供了证据表明它在体外通过 Aurora-A 激酶在苏氨酸 63(T63)位点被磷酸化。我们提出,该位点的磷酸化在被磷酸化时在控制有丝分裂退出中起双重作用,而去磷酸化在果蝇 SL2 细胞中促进 G2/M 转换。