Introduction of a Normal Human Chromosome 8 Corrects Abnormal Phenotypes of Werner Syndrome Cells Immortalized by Expressing an hTERT Gene

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  • ARIYOSHI Kentaro
    Radiation Biology Laboratory, Radiation Research Center, Frontier Science Innovation Center, Organization for University-Industry-Government Cooperation, Osaka Prefecture University Experimental Radiobiology for Children's Health Research Group, Research Center for Radiation Protection, National Institute of Radiological Sciences
  • SUZUKI Keiji
    Course of Life Sciences and Radiation Research, Graduate School of Biomedical Sciences, Nagasaki University
  • GOTO Makoto
    Division of Anti-Ageing and Longevity Sciences, Faculty of Biomedical Engineering, Toin University of Yokohama
  • OSHIMURA Mitsuo
    Division of Molecular Genetics and Biofunction, Department of Biomedical Science, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Sciences, Tottori University
  • ISHIZAKI Kanji
    Central Laboratory and Radiation Biology, Research Institute, Aich Cancer Center
  • WATANABE Masami
    Laboratory of Radiation Biology, Research Reactor Institute, Kyoto University
  • KODAMA Seiji
    Radiation Biology Laboratory, Radiation Research Center, Frontier Science Innovation Center, Organization for University-Industry-Government Cooperation, Osaka Prefecture University

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Werner syndrome (WS) is an autosomal recessive disease characterized by premature aging and caused by mutations of the WRN gene mapped at 8p12. To examine functional complementation of WS phenotypes, we introduced a normal human chromosome 8 into a strain of WS fibroblasts (WS3RGB) immortalized by expressing a human telomerase reverse transcriptase subunit (hTERT) gene. Here, we demonstrate that the abnormal WS phenotypes including cellular sensitivities to 4-nitroquinoline-1-oxide (4NQO) and hydroxy urea (HU), and chromosomal radiosensitivity at G2 phase are corrected by expression of the WRN gene mediated by introducing a chromosome 8. This indicates that those multiple abnormal WS phenotypes are derived from a primary, but not secondary, defect in the WRN gene.

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