NDLI: The human decatenation checkpoint

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The human decatenation checkpoint

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The human decatenation checkpoint

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Piwnica-worms, H. Paules, R. S. Downes, C. S. Kaufmann, W. K. Graves, P. R. Deming, P. B. Cistulli, C. A. Zhao, H.
Description	Author Affiliation: Deming PB ( Department of Pathology and Laboratory Medicine and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.);
Abstract	Chromatid catenation is actively monitored in human cells, with progression from G(2) to mitosis being inhibited when chromatids are insufficiently decatenated. Mitotic delay was quantified in normal and checkpoint-deficient human cells during treatment with ICRF-193, a topoisomerase II catalytic inhibitor that prevents chromatid decatenation without producing topoisomerase-associated DNA strand breaks. Ataxia telangiectasia (A-T) cells, defective in DNA damage checkpoints, showed normal mitotic delay when treated with ICRF-193. The mitotic delay in response to ICRF-193 was ablated in human fibroblasts expressing an ataxia telangiectasia mutated- and rad3-related (ATR) kinase-inactive ATR allele (ATR(ki)). BRCA1-mutant HCC1937 cells also displayed a defect in ICRF-193-induced mitotic delay, which was corrected by expression of wild-type BRCA1. Phosphorylations of hCds1 or Chk1 and inhibition of Cdk1 kinase activity, which are elements of checkpoints associated with DNA damage or replication, did not occur during ICRF-193-induced mitotic delay. Over-expression of cyclin B1 containing a dominant nuclear localization signal, and inhibition of Crm1-mediated nuclear export, reversed ICRF-193-induced mitotic delay. In combination, these results imply that ATR and BRCA1 enforce the decatenation G(2) checkpoint, which may act to exclude cyclin B1/Cdk1 complexes from the nucleus. Moreover, induction of ATR(ki) produced a 10-fold increase in chromosomal aberrations, further emphasizing the vital role for ATR in genetic stability.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	21
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	BRCA1 Protein Metabolism CDC2 Protein Kinase Cell Cycle Proteins Cyclin B Mitosis Physiology Protein-Serine-Threonine Kinases Signal Transduction Topoisomerase II Inhibitors Ataxia Telangiectasia Ataxia Telangiectasia Mutated Proteins Cell Line Cell Nucleus Checkpoint Kinase 2 Cyclin B1 DNA-Binding Proteins G2 Phase Drug Effects Phosphorylation Piperazines Pharmacology Protein Kinases Tumor Suppressor Proteins Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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