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Related Experiment Videos

ATM is required for efficient recombination between immunoglobulin switch regions.

Bernardo Reina-San-Martin1, Hua Tang Chen, André Nussenzweig

  • 1Howard Hughes Medical Institute, The Rockefeller University, 1230 York Ave., New York, NY 10021, USA.

The Journal of Experimental Medicine
|November 3, 2004
PubMed
Summary

Ataxia telangiectasia mutated (ATM) kinase is essential for DNA repair and cell cycle checkpoints. This study reveals ATM is required for efficient immunoglobulin class switch recombination (CSR), impacting antibody production.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • Ataxia telangiectasia mutated (ATM) kinase is crucial for DNA double-strand break repair and cell cycle control.
  • ATM deficiency causes immunodeficiency with low antibody titers, but its role in immunoglobulin gene diversification is unclear.

Purpose of the Study:

  • To investigate the role of ATM in antigen-driven immunoglobulin gene diversification, specifically somatic hypermutation and class switch recombination (CSR).

Main Methods:

  • Assessed ATM's role in somatic hypermutation and CSR in relevant cellular or animal models.
  • Analyzed switch region transcription, accessibility, DNA damage checkpoint protein recruitment, and recombination events.

Main Results:

  • ATM is dispensable for somatic hypermutation.

Related Experiment Videos

  • ATM is required for efficient class switch recombination (CSR).
  • The CSR defect is linked to impaired long-range inter-switch region recombination, not transcription or accessibility, suggesting a role in synapsis.

    • Conclusions:

    • ATM plays a critical, previously unrecognized role in facilitating switch region synapsis during class switch recombination (CSR).
    • This finding clarifies ATM's function in adaptive immunity beyond DNA repair and checkpoint control.