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Let it go: how to deal with a breakup in mitosis

Nature Structural & Molecular Biology volume 21, pages 433–435 (2014)Cite this article

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A new report reveals how mammalian cells silence the DNA-damage response during mitosis to allow cell division to be completed in the presence of DNA lesions.

In response to DNA double-strand breaks (DSBs), a set of proteins accumulate in the proximity of the damage site to form punctate structures termed ionizing radiation–induced foci (IRIFs)1. IRIFs promote DNA repair and trigger checkpoints that block cell-cycle progression to either facilitate repair of the damage or, if the damage is beyond repair, to induce programmed cell death. Failures in the DNA-damage response (DDR) pathway are costly, resulting in the accumulation of mutations, aneuploidy and, ultimately, malignant transformation. However, this process must be tightly regulated to keep IRIFs confined to DNA lesions in order to prevent aberrant DNA repair1.

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Figure 1: Inhibition of recruitment of RNF8 and 53BP1 to DSBs during mitosis.
Figure 2: Mitotic DSB repair causes telomere fusions.

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Authors and Affiliations

  1. Eros Lazzerini Denchi and Julia Li are at the Department of Molecular and Experimental Medicine, Scripps Research Institute, La Jolla, California, USA.,

    Eros Lazzerini Denchi & Julia Li

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  1. Eros Lazzerini Denchi
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  2. Julia Li
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Correspondence to Eros Lazzerini Denchi.

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Denchi, E., Li, J. Let it go: how to deal with a breakup in mitosis. Nat Struct Mol Biol 21, 433–435 (2014). https://doi.org/10.1038/nsmb.2825

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