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Updated: Jul 9, 2026

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

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Breaking down cell cycle checkpoints and DNA repair during antigen receptor gene assembly

E Callén1, M C Nussenzweig, A Nussenzweig

  • 1Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1360, USA. callene@mail.nih.gov

Oncogene
|December 11, 2007
PubMed

Insights

ATM protein prevents lymphocytes from adapting to DNA damage. It maintains genome integrity by halting proliferation of cells with damaged chromosomes, crucial for preventing genomic instability.

Area of Science:

  • Molecular Biology
  • Genetics
  • Immunology

Background:

  • Double-strand breaks (DSBs) are critical DNA lesions.
  • ATM is a key protein in DNA damage response pathways.
  • Lymphocytes can tolerate DSBs and chromosomal aberrations.

Purpose of the Study:

  • To review the role of ATM in preventing lymphocyte adaptation to DNA damage.
  • To discuss ATM's genome maintenance functions.
  • To understand lymphocyte survival despite genomic instability.

Main Methods:

  • Literature review of ATM's role in DNA repair and genome maintenance.
  • Analysis of V(D)J recombination and chromosomal translocations in lymphocytes.
  • Examination of ATM-deficient lymphocyte behavior in vitro and in vivo.

Main Results:

  • ATM-deficient lymphocytes can survive and proliferate with damaged chromosomes.
  • ATM mediates two functions that prevent adaptation to persistent DNA damage.
  • These functions are essential for maintaining lymphocyte genome stability.

Conclusions:

  • ATM plays a vital role in preventing lymphocytes from adapting to DNA damage.
  • ATM's functions are crucial for halting proliferation of cells with compromised genomes.
  • Understanding ATM's role is key to preventing genomic instability in lymphocytes.

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