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

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 () and Ian D. Hickson ()
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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
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
Tian-Neng Li: National Tsing Hua University
Timea Palmai-Pallag: Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford
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
Ian D. Hickson: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms9962

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