Eukaryotic cells have evolved a variety of parallel and redundant DNA damage 
response pathways that function in a coordinated fashion to prevent the fixation 
of DNA damage as mutations. Despite the wealth of knowledge on DNA damage 
signaling on downstream cellular events, the mechanisms of DNA damage 
recognition, DNA repair as well as DNA damage signaling in the context of 
chromatin is poorly understood. Chromodomain helicase DNA-binding proteins (CHD) 
belong to a group of highly conserved chromatin remodeling proteins that are 
implicated in regulation of transcription. In an effort to understand the 
physiological role of one of the CHD members in a mammalian model system, we 
developed a mutant mouse model for the Chd2 gene. The Chd2 mutant mice are 
highly susceptible to spontaneous lymphoid tumor formation. In this study, we 
present evidence that the Chd2 mutant cells are defective in their ability to 
repair DNA damage induced by ionizing and ultraviolet radiation. Consistent with 
the role of Chd2 in regulating DNA damage responses, the Chd2 mutant cells are 
also sensitive to DNA damaging agents in clonogenic assays. In summary, our data 
suggest that the Chd2 protein is involved in regulating the DNA damage responses 
at the chromatin level.