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Related Experiment Video

Updated: Jul 15, 2026

Quantification of γH2AX Foci in Response to Ionising Radiation

Quantification of γH2AX Foci in Response to Ionising Radiation

Published on: April 6, 2010

Genomic instability in mice lacking histone H2AX.

Arkady Celeste¹, Simone Petersen, Peter J Romanienko

¹Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.

Science (New York, N.Y.)

|April 6, 2002

Summary

Histone H2AX is crucial for DNA repair. Mice lacking H2AX exhibit radiation sensitivity, infertility, and impaired DNA repair complex assembly, highlighting its vital role in maintaining genomic stability.

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Last Updated: Jul 15, 2026

Quantification of γH2AX Foci in Response to Ionising Radiation

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Published on: April 6, 2010

Evaluation of the Spatial Distribution of γH2AX following Ionizing Radiation

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Capturing Common Fragile Site Breaks by Native γH2A.X ChIP

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Published on: January 24, 2025

Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

Higher-order chromatin structure can impede DNA damage recognition and repair.
Phosphorylation of histone H2AX at double-strand breaks (DSBs) is linked to the recruitment of DNA repair factors.

Purpose of the Study:

To investigate the physiological role of histone H2AX in DNA damage response and repair.
To determine the consequences of H2AX deficiency in vivo.

Main Methods:

Generation and analysis of H2AX knockout (H2AX-/-) mice.
Assessment of radiation sensitivity, cell-cycle checkpoints, DNA repair capacity, and recruitment of repair factors to DNA damage sites.

Main Results:

H2AX-/- mice displayed radiation sensitivity, growth retardation, immune deficiency, and male infertility.
Chromosomal instability and DNA repair defects were observed in H2AX-/- mice.
Impaired recruitment of Nbs1, 53bp1, and Brca1 to irradiation-induced foci was noted, while Rad51 recruitment remained unaffected.

Conclusions:

Histone H2AX plays a critical role in facilitating the assembly of specific DNA repair complexes at sites of DNA damage.
H2AX is essential for maintaining genomic stability and normal physiological functions, despite not being required for irradiation-induced cell-cycle checkpoints.