ArticleThe Journal of biological chemistry2015
Mammalian Polo-like kinase 1 (Plk1) promotes proper chromosome segregation by phosphorylating and delocalizing the PBIP1·CENP-Q complex from kinetochores.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Identification of Natural Flavonoids Targeting PLK-1 as Potential Anti-Metastatic Agents: A Computational Approach.International journal of molecular sciences · 2026Article
- Bora, CEP192 and Cenexin regulate distinct Plk1-dependent cell and centrosome cycle transitions.Nature communications · 2026Article
- Recent Progress on the Localization of PLK1 to the Kinetochore and Its Role in Mitosis.International journal of molecular sciences · 2022Review
- Comprehensive Analysis of the Expression and Prognostic Significance of the CENP Family in Breast Cancer.International journal of general medicine · 2022Article
- A dimerization-dependent mechanism regulates enzymatic activation and nuclear entry of PLK1.Oncogene · 2022Article
- The Role of Mitotic Kinases and the RZZ Complex in Kinetochore-Microtubule Attachments: Doing the Right Link.Frontiers in cell and developmental biology · 2022Review
- Differential requirements for the CENP-O complex reveal parallel PLK1 kinetochore recruitment pathways.Molecular biology of the cell · 2021Article
- Deciphering the performance of polo-like kinase 1 in triple-negative breast cancer progression according to the centromere protein U-phosphorylation pathway.American journal of cancer research · 2021Article
- Polo kinase recruitment via the constitutive centromere-associated network at the kinetochore elevates centromeric RNA.PLoS genetics · 2020Article
- RZZ-SPINDLY-DYNEIN: you got to keep 'em separated.Cell cycle (Georgetown, Tex.) · 2020Review
- The methyltransferase SETD6 regulates Mitotic progression through PLK1 methylation.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Regulating a key mitotic regulator, polo-like kinase 1 (PLK1).Cytoskeleton (Hoboken, N.J.) · 2018Review
- Centromere protein U facilitates metastasis of ovarian cancer cells by targeting high mobility group box 2 expression.American journal of cancer research · 2018Article
- The equilibrium of ubiquitination and deubiquitination at PLK1 regulates sister chromatid separation.Cellular and molecular life sciences : CMLS · 2017Review
- Insulin Signaling Regulates the FoxM1/PLK1/CENP-A Pathway to Promote Adaptive Pancreatic β Cell Proliferation.Cell metabolism · 2017Article
- Kinetochore assembly and function through the cell cycle.Chromosoma · 2016Review
- Decoding Polo-like kinase 1 signaling along the kinetochore-centromere axis.Nature chemical biology · 2016Article
- Caenorhabditis elegans polo-like kinase PLK-1 is required for merging parental genomes into a single nucleus.Molecular biology of the cell · 2015Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mammalian Plk1 is critically required for proper M phase progression. Plk1 is self-recruited to prekinetochores/kinetochores by phosphorylating and binding to the Thr-78 motif of a kinetochore scaffold protein, PBIP1 (also called CENP-U/50), which forms a stable complex with another kinetochore component, CENP-Q. However, the mechanism regulating Plk1 localization to this site remains largely unknown. Here, we demonstrate that the PBIP1·CENP-Q complex became hyperphosphorylated and rapidly delocalized from kinetochores as cells entered mitosis. Plk1 phosphorylated the CENP-Q subunit of the PBIP1·CENP-Q complex at multiple sites, and mutation of nine Plk1-dependent phosphorylation sites to Ala (9A) enhanced CENP-Q association with chromatin and prolonged CENP-Q localization to kinetochores. Conversely, mutation of the nine sites to phospho-mimicking Asp/Glu (9D/E) residues dissociated CENP-Q from chromatin and kept the CENP-Q(9D/E) mutant from localizing to interphase prekinetochores. Strikingly, both the 9A and 9D/E mutants induced a defect in proper chromosome segregation, suggesting that both timely localization of the PBIP1·CENP-Q complex to prekinetochores and delocalization from kinetochores are critical for normal M phase progression. Notably, although Plk1 did not alter the level of PBIP1 and CENP-Q ubiquitination, Plk1-dependent phosphorylation and delocalization of these proteins from kinetochores appeared to indirectly lead to their degradation in the cytosol. Thus, we propose that Plk1 regulates the timing of the delocalization and ultimate destruction of the PBIP1·CENP-Q complex and that these processes are important not only for promoting Plk1-dependent mitotic progression, but also for resetting the timing of Plk1 recruitment to prekinetochores in the next cell cycle.
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