Replication stress activates DNA repair synthesis in mitosis

Sheroy Minocherhomji, Songmin Ying, Victoria A. Bjerregaard, Sara Bursomanno, Aiste Aleliunaite, Wei Wu, Hocine W. Mankouri, Huahao Shen (), Ying Liu () and Ian D. Hickson ()
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Sheroy Minocherhomji: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Songmin Ying: Zhejiang University School of Medicine
Victoria A. Bjerregaard: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Sara Bursomanno: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Aiste Aleliunaite: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Wei Wu: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Hocine W. Mankouri: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Huahao Shen: Zhejiang University School of Medicine
Ying Liu: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute
Ian D. Hickson: Center for Chromosome Stability and Center for Healthy Aging, University of Copenhagen, Panum Institute

Nature, 2015, vol. 528, issue 7581, 286-290

Abstract: Common fragile sites (CFSs) are difficult-to-replicate regions of eukaryotic genomes that are sensitive to replication stress and that require resolution by the MUS81–EME1 endonuclease to re-initiate POLD3-dependent DNA synthesis in early mitosis; this study defines the specific pathway of events causing the CFS fragility phenotype.

Date: 2015
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DOI: 10.1038/nature16139

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