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PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis

Author

Listed:
  • Christian F. Nielsen

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen)

  • Diana Huttner

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen
    Center for Protein Research, University of Copenhagen
    Present address: Department of Biomedical Engineering, Technion - Israel Institute of Technology, 32000 Haifa, Israel)

  • Anna H. Bizard

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen)

  • Seiki Hirano

    (Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford
    Present address: Department of Endocrinology, Metabolism and Nephrology, Kochi Medical School, Kochi University, 7838505, Japan)

  • Tian-Neng Li

    (National Tsing Hua University)

  • Timea Palmai-Pallag

    (Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford
    Present address: School of Life Sciences, University of Lincoln, LN6 7DL Lincoln, UK)

  • Victoria A. Bjerregaard

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen)

  • Ying Liu

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen)

  • Erich A. Nigg

    (Biozentrum, University of Basel)

  • Lily Hui-Ching Wang

    (National Tsing Hua University
    Biozentrum, University of Basel)

  • Ian D. Hickson

    (Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen
    Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford)

Abstract

PICH is a SNF2 family DNA translocase that binds to ultra-fine DNA bridges (UFBs) in mitosis. Numerous roles for PICH have been proposed from protein depletion experiments, but a consensus has failed to emerge. Here, we report that deletion of PICH in avian cells causes chromosome structural abnormalities, and hypersensitivity to an inhibitor of Topoisomerase II (Topo II), ICRF-193. ICRF-193-treated PICH−/− cells undergo sister chromatid non-disjunction in anaphase, and frequently abort cytokinesis. PICH co-localizes with Topo IIα on UFBs and at the ribosomal DNA locus, and the timely resolution of both structures depends on the ATPase activity of PICH. Purified PICH protein strongly stimulates the catalytic activity of Topo II in vitro. Consistent with this, a human PICH−/− cell line exhibits chromosome instability and chromosome condensation and decatenation defects similar to those of ICRF-193-treated cells. We propose that PICH and Topo II cooperate to prevent chromosome missegregation events in mitosis.

Suggested Citation

  • Christian F. Nielsen & Diana Huttner & Anna H. Bizard & Seiki Hirano & Tian-Neng Li & Timea Palmai-Pallag & Victoria A. Bjerregaard & Ying Liu & Erich A. Nigg & Lily Hui-Ching Wang & Ian D. Hickson, 2015. "PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis," Nature Communications, Nature, vol. 6(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9962
    DOI: 10.1038/ncomms9962
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    Cited by:

    1. Dian Spakman & Tinka V. M. Clement & Andreas S. Biebricher & Graeme A. King & Manika I. Singh & Ian D. Hickson & Erwin J. G. Peterman & Gijs J. L. Wuite, 2022. "PICH acts as a force-dependent nucleosome remodeler," Nature Communications, Nature, vol. 13(1), pages 1-12, December.

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