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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

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RNF168 forms a functional complex with RAD6 during the DNA damage response.

Chao Liu¹, Degui Wang, Jiaxue Wu

¹State Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, 200433, China.

Journal of Cell Science

|March 26, 2013

Summary

This summary is machine-generated.

RAD6A and RAD6B enzymes work with RNF168 to initiate DNA damage response ubiquitination. Their absence impairs DNA repair protein recruitment and foci formation after ionizing radiation.

Keywords:

DNA damage response RAD6 RNF168 Ubiquitination

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Area of Science:

Molecular Biology
Cellular Biology
Biochemistry

Background:

Protein ubiquitination is vital for the DNA damage response.
E2 ubiquitin conjugating enzymes catalyze ubiquitination, recruiting DNA repair factors to lesions.

Purpose of the Study:

Identify novel E2 conjugating enzymes in the DNA-damage-induced ubiquitination cascade.
Investigate the roles of RAD6A and RAD6B in response to ionizing radiation (IR).

Main Methods:

Screening of known E2 enzymes.
Analysis of RAD6A/RAD6B-deficient cells and RNF168-deficient cells.
In vitro and in vivo ubiquitination assays targeting histone H1.2.

Main Results:

RAD6A and RAD6B were found to function with RNF168 in the IR-induced DNA damage response.
Absence of RAD6A or RAD6B reduced DNA-damage-induced protein ubiquitination and foci formation of BRCA1 and 53BP1.
The RNF168-RAD6 complex ubiquitinated histone H1.2 in vitro and regulated its ubiquitination in vivo.

Conclusions:

RNF168, complexed with RAD6A or RAD6B, is activated in the DNA-damage-induced protein ubiquitination cascade.
RAD6A and RAD6B are crucial E2 enzymes for initiating the DNA damage response pathway.