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Cell cycle

Fools rush in

Nature volume 401, pages 535–536 (1999)Cite this article

The cell-division cycle is the means by which cells accurately duplicate themselves and then divide in two. In recent years a general model has emerged in which protein complexes consisting of cyclins and cyclin-dependent protein kinases (Cdks) regulate progression through this cycle1. In addition, ‘checkpoints’ exist to monitor the integrity and replication status of the genetic material before cells commit either to replicate their DNA (in S phase) or to segregate it (during mitosis)2. These checkpoints are signal-transduction pathways whose effectors interact with cyclin/Cdk complexes to block the cell cycle. A report by Chan et al.3 on page 616 of this issue helps us to understand how checkpoints do this.

Why the need to block the cell-division cycle? If DNA is damaged, a delay in the cell cycle facilitates repair, minimizing the replication and subsequent segregation of damaged DNA. Indeed, loss of checkpoint integrity is a hallmark of many human cancers4. Cells respond to DNA damage by stopping the cell cycle either at a stage known as G1, before DNA replication (via the G1 DNA-damage checkpoint), or just before mitosis by the G2 DNA-damage checkpoint.

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Figure 1: Cellular response to DNA damage.

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Authors and Affiliations

  1. Department of Cell Biology and Physiology, Howard Hughes Medical Institute, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, 63110-1093, Missouri, USA

    Helen Piwnica-Worms

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  1. Helen Piwnica-Worms
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Correspondence to Helen Piwnica-Worms.

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Piwnica-Worms, H. Fools rush in. Nature 401, 535–536 (1999). https://doi.org/10.1038/44029

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