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Involvement of the chromatin remodeling factors CHD4 in the DNA damage response

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DNA damage can induced genome instability, cell senescence or cell death if they are not repaired properly. DNA repair pathways guarantee the integrity and the fidelity of the genome information. The arrest or delay of cell cycle progression is also essential when DNA lesions occur. This is ensured by checkpoint pathways that crosstalk with DNA repair and the cell cycle pogression machineries. DNA damage must be detected and repaired in the context of chromatin. The chromatin structure is thought critical for DNA lesions detection, checkpoints activation, DNA repair, damage-induced transcription. Several chromatin-modifying and chromatin remodeling factors were shown involved in the DNA damage response. However chromatin modifications and their consequences during DNA damage responses are poorly understood.

The chromodomain helicase DNA binding protein 4 (CHD4) is an ATP depend chromatin remodeling factor mainly described as an autoantigen in some myositis and a component of the nucleosome remodeling and histone deacetylase complex, which is a negative regulator of transcription. Several studies link CHD4 with cell proliferation. Futhermore CHD4 has been reported interacting with ATR and identified as a potential substrate of the checkpoint kinases ATM and/or ATR after ionizing radiation (IR). These literature data suggest that CHD4 may play a role in the cellular response to DNA damage. First we investigate if CHD4 could localize to or participate in the formation of the IR-induced foci (IR), that are microscopically discernible structures ocurring in the vicinity of the lesions. We show that CHD4 is not recruited to the IRIF. We also studied the influence of CHD4 down-regulation with the siRNA technology on the formation of the IRIF. In CHD4 down-regulated cells appeareance of phosphorylated histone H2AX foci seems to be similar to the RNAi control treated cells as the recruitment of well-known DNA repair factors. Our data indicate that CHD4 protein isn't a component of the IRIF and doesn't participate (at least at a detectable level) in their formation. We confirmed the phosphorylation of CHD4 after DNA damage. We are currently investigating if CHD4 can be involved in the checkpoint pathways.
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Document Type: Abstract

Affiliations: Centre for Genotoxic Stress Research, Institute of Cancer Biology, Danish Cancer Society, Denmark

Publication date: May 1, 2008

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