ArticleNature communications2015
CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 114 citations in OpenAlex.
- Basal body docking failure triggers centriole clustering and elimination in mammalian spermatogenesis.EMBO reports · 2026Article
- Mechanical constraints regulate embryonic stem cell mitosis in the developing brain.The EMBO journal · 2026Article
- Centriole Duplication, Maturation, and Transformation During Mammalian Spermatogenesis.Advances in experimental medicine and biology · 2026Review
- Recessive variants in WSB2 encoding a substrate receptor of E3 ubiquitin ligase underlie a neurodevelopmental syndrome.European journal of human genetics : EJHG · 2026Article
- Loss of cilia drives centriole clustering and elimination during mammalian spermatogenesis.bioRxiv : the preprint server for biology · 2025Article
- Meiotic divisions and round spermatid formation do not require centriole duplication in mice.PLoS genetics · 2025Article
- Loss of Cep135 causes oligoasthenoteratozoospermia and male infertility in mice.Cellular and molecular life sciences : CMLS · 2025Article
- Developmental and tissue-specific roles of mammalian centrosomes.The FEBS journal · 2025Review
- Spermatocytes have the capacity to segregate chromosomes despite centriole duplication failure.EMBO reports · 2024Article
- A proteomics approach to isolating neuropilin-dependent α5 integrin trafficking pathways: neuropilin 1 and 2 co-traffic α5 integrin through endosomal p120RasGAP to promote polarised fibronectin fibrillogenesis in endothelial cells.Communications biology · 2024Article
- Control of cell proliferation by memories of mitosis.Science (New York, N.Y.) · 2024Article
- The AP-2 complex interacts with γ-TuRC and regulates the proliferative capacity of neural progenitors.Life science alliance · 2024Article
- The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.Scientific reports · 2024Article
- Aberrant generation of dentate gyrus granule cells is associated with epileptic susceptibility in p53 conditional knockout mice.Frontiers in neuroscience · 2024Article
- Regulation of p53 by the mitotic surveillance/stopwatch pathway: implications in neurodevelopment and cancer.Frontiers in cell and developmental biology · 2024Review
- Radial glia progenitor polarity in health and disease.Frontiers in cell and developmental biology · 2024Review
- What happens to the osteoporotic bone mesenchymal stem cells? Evidence from RNA sequencing.International journal of medical sciences · 2024Article
- Architectural basis for cylindrical self-assembly governing Plk4-mediated centriole duplication in human cells.Communications biology · 2023Article
- Distinct dynein complexes defined by DYNLRB1 and DYNLRB2 regulate mitotic and male meiotic spindle bipolarity.Nature communications · 2023Article
- An entosis-like process induces mitotic disruption in Pals1 microcephaly pathogenesis.Nature communications · 2023Article
12 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 6 institutions in 4 countries.
Funding
Abstract
CEP63 is a centrosomal protein that facilitates centriole duplication and is regulated by the DNA damage response. Mutations in CEP63 cause Seckel syndrome, a human disease characterized by microcephaly and dwarfism. Here we demonstrate that Cep63-deficient mice recapitulate Seckel syndrome pathology. The attrition of neural progenitor cells involves p53-dependent cell death, and brain size is rescued by the deletion of p53. Cell death is not the result of an aberrant DNA damage response but is triggered by centrosome-based mitotic errors. In addition, Cep63 loss severely impairs meiotic recombination, leading to profound male infertility. Cep63-deficient spermatocytes display numerical and structural centrosome aberrations, chromosome entanglements and defective telomere clustering, suggesting that a reduction in centrosome-mediated chromosome movements underlies recombination failure. Our results provide novel insight into the molecular pathology of microcephaly and establish a role for the centrosome in meiotic recombination.
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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.