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    A centrosome-autonomous signal that involves centriole disengagement permits centrosome duplication in G2 phase after DNA damage.

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    Authors
    Inanç, Burcu
    Dodson, Helen
    Morrison, Ciaran G
    Affiliation
    Centre for Chromosome Biology, School of Natural Sciences, National University of Ireland Galway, Galway, Ireland.
    Issue Date
    2010-11-15
    MeSH
    Animals
    Calcium-Binding Proteins
    Cell Cycle
    Cell Cycle Proteins
    Cell Line, Tumor
    Centrioles
    Centrosome
    DNA Damage
    G2 Phase
    Humans
    Immunoblotting
    Luminescent Proteins
    Microscopy, Fluorescence
    Microtubule-Associated Proteins
    Proliferating Cell Nuclear Antigen
    S Phase
    Signal Transduction
    Time Factors
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    Citation
    A centrosome-autonomous signal that involves centriole disengagement permits centrosome duplication in G2 phase after DNA damage. 2010, 21 (22):3866-77 Mol. Biol. Cell
    Journal
    Molecular biology of the cell
    URI
    http://hdl.handle.net/10147/125266
    DOI
    10.1091/mbc.E10-02-0124
    PubMed ID
    20861312
    Abstract
    DNA damage can induce centrosome overduplication in a manner that requires G2-to-M checkpoint function, suggesting that genotoxic stress can decouple the centrosome and chromosome cycles. How this happens is unclear. Using live-cell imaging of cells that express fluorescently tagged NEDD1/GCP-WD and proliferating cell nuclear antigen, we found that ionizing radiation (IR)-induced centrosome amplification can occur outside S phase. Analysis of synchronized populations showed that significantly more centrosome amplification occurred after irradiation of G2-enriched populations compared with G1-enriched or asynchronous cells, consistent with G2 phase centrosome amplification. Irradiated and control populations of G2 cells were then fused to test whether centrosome overduplication is allowed through a diffusible stimulatory signal, or the loss of a duplication-inhibiting signal. Irradiated G2/irradiated G2 cell fusions showed significantly higher centrosome amplification levels than irradiated G2/unirradiated G2 fusions. Chicken-human cell fusions demonstrated that centrosome amplification was limited to the irradiated partner. Our finding that only the irradiated centrosome can duplicate supports a model where a centrosome-autonomous inhibitory signal is lost upon irradiation of G2 cells. We observed centriole disengagement after irradiation. Although overexpression of dominant-negative securin did not affect IR-induced centrosome amplification, Plk1 inhibition reduced radiation-induced amplification. Together, our data support centriole disengagement as a licensing signal for DNA damage-induced centrosome amplification.
    Item Type
    Article
    Language
    en
    ISSN
    1939-4586
    ae974a485f413a2113503eed53cd6c53
    10.1091/mbc.E10-02-0124
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