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ATM controls meiotic double-strand-break formation

Author

Listed:
  • Julian Lange

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center)

  • Jing Pan

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center
    Present address: Cell Biology Department, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.)

  • Francesca Cole

    (Developmental Biology Program, Memorial Sloan-Kettering Cancer Center)

  • Michael P. Thelen

    (Physical and Life Sciences Directorate, Lawrence Livermore National Laboratory)

  • Maria Jasin

    (Developmental Biology Program, Memorial Sloan-Kettering Cancer Center)

  • Scott Keeney

    (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center
    Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center)

Abstract

Keeping a cap on DNA strand breakage During meiosis, a limited number of double-strand breaks are made in the DNA by Spo11 protein to facilitate correct chromosome segregation. The level of Spo11 is in considerable excess to the number of strand breaks that are made, suggesting that some mechanism is at work to limit its activity. Scott Keeney and colleagues show that ATM kinase, which has a central role in repair of spontaneous double-strand breaks, also functions in a feedback loop to restrain meiotic strand breakage.

Suggested Citation

  • Julian Lange & Jing Pan & Francesca Cole & Michael P. Thelen & Maria Jasin & Scott Keeney, 2011. "ATM controls meiotic double-strand-break formation," Nature, Nature, vol. 479(7372), pages 237-240, November.
    • Handle: RePEc:nat:nature:v:479:y:2011:i:7372:d:10.1038_nature10508
    DOI: 10.1038/nature10508
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