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CELL CYCLE

A(TR) checkpoint for S/G2 transition

Nature Reviews Molecular Cell Biology volume 19, pages 676–677 (2018)Cite this article

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Each phase of the cell cycle must be completed before the next phase can start, to ensure the integrity of the genetic information passed on to the daughter cells. Serine/threonine-protein kinase ATR is activated when DNA damage occurs, leading to cell cycle arrest in S phase or G2 phase. A study in Science now reports that ATR is a potential sensor of the completion of DNA replication during normal cell cycle and the driver of S phase to G2 phase (S/G2) transition.

Mining of public chromatin immunoprecipitation (ChIP) sequencing data revealed that the mitotic transcription factors B-MYB and forkhead box protein M1 (FOXM1) were enriched at the promoters of these genes, and cyclin B accumulation in ATRi-treated cells was inhibited by FOXM1 depletion. In line with this finding, FOXM1 phosphorylation at Thr600 — which was found to be carried out by cyclin A–CDK1 — and consequently FOXM1 activation was increased to G2 levels prematurely and in a switch-like manner in ATRi-treated S phase cells.

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References

Original article

  • Saldivar, J. C. et al. An intrinsic S/G2 checkpoint enforced by ATR. Science 361, 806–810 (2018)

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Further reading

  • Saldivar, J. C. et al. The essential kinase ATR: ensuring faithful duplication of a challenging genome. Nat. Rev. Mol. Cell Biol. 18, 622–636 (2017)

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  1. Associate Editor, Nature Communications http://www.nature.com/nrm/

    Michelle Trenkmann

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  1. Michelle Trenkmann
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Correspondence to Michelle Trenkmann.

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Trenkmann, M. A(TR) checkpoint for S/G2 transition. Nat Rev Mol Cell Biol 19, 676–677 (2018). https://doi.org/10.1038/s41580-018-0064-4

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  • DOI: https://doi.org/10.1038/s41580-018-0064-4

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