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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

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Chfr and RNF8 synergistically regulate ATM activation.

Jiaxue Wu¹, Yibin Chen, Lin-Yu Lu

¹Division of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA.

Nature Structural & Molecular Biology

|June 28, 2011

Summary

RNF8 and Chfr E3 ligases are crucial for DNA damage response. Their combined loss suppresses ATM activation, leading to genomic instability and cancer in mice.

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Area of Science:

Molecular Biology
Genetics
Biochemistry

Background:

Protein ubiquitination is vital for DNA damage response.
E3 ubiquitin ligases play key roles in this process.

Purpose of the Study:

To investigate the roles of RNF8 and Chfr in DNA damage-induced ubiquitination.
To elucidate their impact on ATM kinase activation and genomic stability.

Main Methods:

Analysis of RNF8 and Chfr knockout (DKO) cells and mice.
Assessment of ATM kinase activation and DNA damage response pathways.
Investigation of histone ubiquitination and acetylation dynamics.

Main Results:

DKO cells exhibit suppressed ATM activation and hypersensitivity to ionizing radiation.
DKO mice develop thymic lymphomas with chromosome translocations.
RNF8 and Chfr synergistically regulate histone H4 Lys16 acetylation via MRG15-dependent complexes.

Conclusions:

RNF8 and Chfr act synergistically to modulate chromatin relaxation and ATM activation.
These chromatin-remodeling factors are essential for maintaining genomic stability in vivo.