Ablation of PARP-1 does not interfere with the repair of DNA double-strand breaks, but compromises the reactivation of stalled replication forks.
作者： Yun-Gui Yang , Ulrich Cortes , Srinivas Patnaik , Maria Jasin , Zhao-Qi Wang
关键词: Control of chromosome duplication 、 DNA 、 Homologous recombination 、 DNA repair 、 Molecular biology 、 DNA damage 、 Replication protein A 、 RAD51 、 Biology 、 DNA replication
摘要: Poly(ADP-ribose) polymerase-1 (PARP-1) is an abundant DNA end-sensing and binding molecule. Inactivation of PARP-1 by chemicals genetic mutations slows cell proliferation, increases sister chromatid exchange (SCE), micronuclei formation chromosome instability, shortens telomeres. Given its affinity to breaks temporal occupation on strand break sites, proposed prevent inappropriate recombination. We investigated the potential role in repair double-strand (DSBs) stalled replication forks. PARP-1-/- embryonic stem cells fibroblast exhibited normal DSBs either homologous recombination (HR) or nonhomologous end-joining (NHEJ) pathways. did not interfere with gene-targeting efficiency ES cells. However, were hypersensitive damage agent hydroxyurea (HU)-induced death enhanced SCE formation. Ablation delayed reactivation forks imposed HU re-entry into G2-M phase after release. These data indicate that dispensable HR induced DSBs, but involved
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