ArticleNature communications2017
Precocious centriole disengagement and centrosome fragmentation induced by mitotic delay.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Kinetochore-centrosome feedback linking CENP-E and Aurora kinases controls chromosome congression.Nature communications · 2025Article
- 14-3-3ε inhibits premature centriole disengagement by inhibiting the activity of Plk1 and separase.Journal of cell science · 2025Article
- M phase-specific generation of supernumerary centrioles in cancer cells.Molecular biology of the cell · 2025Article
- Factors that determine cell fate in mitotically arrested cancer cells.Frontiers in cell and developmental biology · 2025Article
- MLL/WDR5 complex recruits centriolar satellite protein Cep72 to regulate microtubule nucleation and spindle formation.Science advances · 2024Article
- Centrosome linker diversity and its function in centrosome clustering and mitotic spindle formation.The EMBO journal · 2023Article
- Distinct dynein complexes defined by DYNLRB1 and DYNLRB2 regulate mitotic and male meiotic spindle bipolarity.Nature communications · 2023Article
- Piezo mechanosensory channels regulate centrosome integrity and mitotic entry.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Role of Polo-like Kinases Plk1 and Plk4 in the Initiation of Centriole Duplication-Impact on Cancer.Cells · 2022Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Article
- Characterization of a recently synthesized microtubule-targeting compound that disrupts mitotic spindle poles in human cells.Scientific reports · 2021Article
- Dysregulation of the centrosome induced by BRCA1 deficiency contributes to tissue-specific carcinogenesis.Cancer science · 2021Review
- Orbit/CLASP determines centriole length by antagonising Klp10A inJournal of cell science · 2021Article
- A non-canonical function for Centromere-associated protein-E controls centrosome integrity and orientation of cell division.Communications biology · 2021Article
- Mild replication stress causes chromosome mis-segregation via premature centriole disengagement.Nature communications · 2019Article
- Inhibition of CPAP-tubulin interaction prevents proliferation of centrosome-amplified cancer cells.The EMBO journal · 2019Article
- Activation of the apoptotic pathway during prolonged prometaphase blocks daughter cell proliferation.Molecular biology of the cell · 2018Article
- Caspase-mediated cleavage of the centrosomal proteins during apoptosis.Cell death & disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The spindle assembly checkpoint (SAC) delays mitotic progression until all sister chromatid pairs achieve bi-orientation, and while the SAC can maintain mitotic arrest for extended periods, moderate delays in mitotic progression have significant effects on the resulting daughter cells. Here we show that when retinal-pigmented epithelial (RPE1) cells experience mitotic delay, there is a time-dependent increase in centrosome fragmentation and centriole disengagement. While most cells with disengaged centrioles maintain spindle bipolarity, clustering of disengaged centrioles requires the kinesin-14, HSET. Centrosome fragmentation and precocious centriole disengagement depend on separase and anaphase-promoting complex/cyclosome (APC/C) activity, which also triggers the acquisition of distal appendage markers on daughter centrioles and the loss of procentriolar markers. Together, these results suggest that moderate delays in mitotic progression trigger the initiation of centriole licensing through centriole disengagement, at which point the ability to maintain spindle bipolarity becomes a function of HSET-mediated spindle pole clustering.
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What Socratic holds
Registered trials
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 Socratic graph.