ArticleCurrent biology : CB2014
A unique set of centrosome proteins requires pericentrin for spindle-pole localization and spindle orientation.
Article in Current biology : CB, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 66 papers.
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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.
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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.
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Who cites it
66 citing papers in PubMed, 89 citations in OpenAlex.
- Activating adaptor-like sequences in pericentrin mediate its transport by dynein.bioRxiv : the preprint server for biology · 2026Article
- A Predictive Model for Coupling Cell Division Orientation to Tissue Mechanics During Epithelial Morphogenesis.bioRxiv : the preprint server for biology · 2026Article
- A predictive model for coupling cell division orientation to tissue mechanics during epithelial morphogenesis.Frontiers in cell and developmental biology · 2026Article
- A conserved role for centriolar satellites in translation of centrosomal and ciliary proteins.The Journal of cell biology · 2025Article
- [Microcephalic osteodysplastic primordial dwarfism type II (MOPD II): clinical case].Problemy endokrinologii · 2025Article
- Specific mitotic events drive left-right organizer development.Development (Cambridge, England) · 2025Article
- NE-MTOC Formation in Skeletal Muscle Is Mbnl2-Dependent and Occurs in a Sequential and Gradual Manner.Cells · 2025Article
- Developmental and tissue-specific roles of mammalian centrosomes.The FEBS journal · 2025Review
- SLMAP3 is crucial for organogenesis through mechanisms involving primary cilia formation.Open biology · 2024Article
- Genetic Primary Microcephalies: When Centrosome Dysfunction Dictates Brain and Body Size.Cells · 2023Review
- Quantitative Image Processing for Three-Dimensional Episcopic Images of Biological Structures: Current State and Future Directions.Biomedicines · 2023Review
- Context-Dependent Function of Long Noncoding RNAMolecular and cellular biology · 2022Article
- Pericentriolar matrix (PCM) integrity relies on cenexin and polo-like kinase (PLK)1.Molecular biology of the cell · 2022Article
- Article
- WDR62 variants contribute to congenital heart disease by inhibiting cardiomyocyte proliferation.Clinical and translational medicine · 2022Article
- Orb-dependent polyadenylation contributes to PLP expression and centrosome scaffold assembly.Development (Cambridge, England) · 2022Article
- Genetic resiliency associated with dominant lethalCell reports. Medicine · 2022Article
- Clinical and Genetic Analysis of a Patient With Coexisting 17a-Hydroxylase/17,20-Lyase Deficiency and Moyamoya Disease.Frontiers in genetics · 2022Article
- Article
- Time is of the essence: the molecular mechanisms of primary microcephaly.Genes & development · 2021Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
- Erratum issued
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Majewski osteodysplastic primordial dwarfism type II (MOPDII) is caused by mutations in the centrosome gene pericentrin (PCNT) that lead to severe pre- and postnatal growth retardation. As in MOPDII patients, disruption of pericentrin (Pcnt) in mice caused a number of abnormalities including microcephaly, aberrant hemodynamics analyzed by in utero echocardiography, and cardiovascular anomalies; the latter being associated with mortality, as in the human condition. To identify the mechanisms underlying these defects, we tested for changes in cell and molecular function. All Pcnt(-/-) mouse tissues and cells examined showed spindle misorientation. This mouse phenotype was associated with misdirected ventricular septal growth in the heart, decreased proliferative symmetric divisions in brain neural progenitors, and increased misoriented divisions in fibroblasts; the same phenotype was seen in fibroblasts from three MOPDII individuals. Misoriented spindles were associated with disrupted astral microtubules and near complete loss of a unique set of centrosome proteins from spindle poles (ninein, Cep215, centriolin). All these proteins appear to be crucial for microtubule anchoring and all interacted with Pcnt, suggesting that Pcnt serves as a molecular scaffold for this functionally linked set of spindle pole proteins. Importantly, Pcnt disruption had no detectable effect on localization of proteins involved in the cortical polarity pathway (NuMA, p150(glued), aPKC). Not only do these data reveal a spindle-pole-localized complex for spindle orientation, but they identify key spindle symmetry proteins involved in the pathogenesis of MOPDII.
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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 OpenQuestion graph.