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Aberrant chromosome morphology in human cells defective for Holliday junction resolution

Author

Listed:
  • Thomas Wechsler

    (London Research Institute, Cancer Research UK, Clare Hall Laboratories
    Present address: Stanford University School of Medicine, Clark Center, 318 Campus Drive, Stanford, California 94305, USA.)

  • Scott Newman

    (University of Cambridge)

  • Stephen C. West

    (London Research Institute, Cancer Research UK, Clare Hall Laboratories)

Abstract

Disruption at Holliday junction Exchange of sister chromatids to form four-stranded Holliday junctions occurs naturally during meiosis, to hold sister chromatids together, and during various repair events. In eukaryotes, double Holliday junctions that escape dissolution by a helicase–topoisomerase (BTR) complex are instead processed by one of several nucleases, known as resolvases. In this study, Stephen West and colleagues define the activities of the GEN1, MUS81–EME1 and SLX1–SLX4 resolvases in the absence of BLM, the helicase component of BTR that is mutated in Bloom's syndrome. The use of these alternatives may come at a price, however, because Bloom's syndrome cells exhibit genomic instability and patients experience a broad spectrum of early-onset cancers.

Suggested Citation

  • Thomas Wechsler & Scott Newman & Stephen C. West, 2011. "Aberrant chromosome morphology in human cells defective for Holliday junction resolution," Nature, Nature, vol. 471(7340), pages 642-646, March.
    • Handle: RePEc:nat:nature:v:471:y:2011:i:7340:d:10.1038_nature09790
    DOI: 10.1038/nature09790
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    Cited by:

    1. Junliang Chen & Mingjie Wu & Yulan Yang & Chunyan Ruan & Yi Luo & Lizhi Song & Ting Wu & Jun Huang & Bing Yang & Ting Liu, 2024. "TFIP11 promotes replication fork reversal to preserve genome stability," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    2. Laura J. Grange & John J. Reynolds & Farid Ullah & Bertrand Isidor & Robert F. Shearer & Xenia Latypova & Ryan M. Baxley & Antony W. Oliver & Anil Ganesh & Sophie L. Cooke & Satpal S. Jhujh & Gavin S., 2022. "Pathogenic variants in SLF2 and SMC5 cause segmented chromosomes and mosaic variegated hyperploidy," Nature Communications, Nature, vol. 13(1), pages 1-22, December.

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