ArticleNature communications2019
The Cep57-pericentrin module organizes PCM expansion and centriole engagement.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 78 citations in OpenAlex.
- NuSAP Safeguards Centriole Integrity to Mediate CEP57-CEP152 Torus Recruitment for Proper Engagement.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Critical constituents and assembly principles of centriole biogenesis in human cells.Nature reviews. Molecular cell biology · 2026Review
- TRIM37 recognizes a bipartite degron to ubiquitinate centrosome substrates.bioRxiv : the preprint server for biology · 2025Article
- PLK4: Master Regulator of Centriole Duplication and Its Therapeutic Potential.Cytoskeleton (Hoboken, N.J.) · 2025Review
- The DNA replication machinery transmits dual signals to prevent unscheduled licensing and execution of centrosome duplication.Nature communications · 2025Article
- M phase-specific generation of supernumerary centrioles in cancer cells.Molecular biology of the cell · 2025Article
- Mosaic variegated aneuploidy in development, ageing and cancer.Nature reviews. Genetics · 2024Review
- The core spindle pole body scaffold Ppc89 links the pericentrin orthologue Pcp1 to the fission yeast spindle pole body via an evolutionarily conserved interface.Molecular biology of the cell · 2024Article
- Cep57 regulates human centrosomes through multivalent interactions.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Molecular basis promoting centriole triplet microtubule assembly.Nature communications · 2024Article
- Centrosome amplification and aneuploidy driven by the HIV-1-induced Vpr•VprBP•Plk4 complex in CD4Nature communications · 2024Article
- A potential patient stratification biomarker for Parkinson´s disease based on LRRK2 kinase-mediated centrosomal alterations in peripheral blood-derived cells.NPJ Parkinson's disease · 2024Article
- Architectural basis for cylindrical self-assembly governing Plk4-mediated centriole duplication in human cells.Communications biology · 2023Article
- Microcephaly, Short Stature, Intellectual Disability, Speech Absence and Cataract Are Associated with Novel Bi-Allelic Missense Variant inChildren (Basel, Switzerland) · 2023Article
- A Functional Yeast-Based Screen Identifies the Host Microtubule Cytoskeleton as a Target of NumerousInternational journal of molecular sciences · 2023Article
- The physiological and pathological mechanisms of early embryonic development.Fundamental research · 2022Review
- Oncogenic BRAF induces whole-genome doubling through suppression of cytokinesis.Nature communications · 2022Article
- Effects of aneuploidy on cell behaviour and function.Nature reviews. Molecular cell biology · 2022Review
- Role of Polo-like Kinases Plk1 and Plk4 in the Initiation of Centriole Duplication-Impact on Cancer.Cells · 2022Review
- The APC/C targets the Cep152-Cep63 complex at the centrosome to regulate mitotic spindle assembly.Journal of cell science · 2022Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centriole duplication occurs once per cell cycle to ensure robust formation of bipolar spindles and chromosome segregation. Each newly-formed daughter centriole remains connected to its mother centriole until late mitosis. The disengagement of the centriole pair is required for centriole duplication. However, the mechanisms underlying centriole engagement remain poorly understood. Here, we show that Cep57 is required for pericentriolar material (PCM) organization that regulates centriole engagement. Depletion of Cep57 causes PCM disorganization and precocious centriole disengagement during mitosis. The disengaged daughter centrioles acquire ectopic microtubule-organizing-center activity, which results in chromosome mis-segregation. Similar defects are observed in mosaic variegated aneuploidy syndrome patient cells with cep57 mutations. We also find that Cep57 binds to the well-conserved PACT domain of pericentrin. Microcephaly osteodysplastic primordial dwarfism disease pericentrin mutations impair the Cep57-pericentrin interaction and lead to PCM disorganization. Together, our work demonstrates that Cep57 provides a critical interface between the centriole core and PCM.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.