It has been over a quarter century since Drs. Smerdon and Lieberman published their groundbreaking paper demonstrating that significant structural rearrangements occur at the nucleosome level of chromatin during nucleotide excision repair (NER) of DNA damage in human cells (Smerdon and Lieberman, 1978, Proc. Natl. Acad. Sci. USA 75: 4238). Understanding the mechanism(s) of this rearrangement process has been one of the goals of the Smerdon lab ever since. It was clear from the beginning that DNA repair must take place throughout the genome, within all levels of the chromatin packaging hierarchy, since no region within chromatin is fully protected from exogenous and/or endogenous DNA damage. In 1987, the Smerdon lab reported that UV light-Induced DNA damage is strongly modulated by the packaging of DNA into nucleosomes (Gale et al., 1987, Proc. Natl. Acad. Sci. USA  84: 6644). This report helped set the stage for our understanding that both DNA damage and DNA repair can be strongly modulated by the packaging of DNA in chromatin.

            New technological advances led to a more comprehensive understanding of these findings, and during the past decade there was a significant increase in research focused directly on DNA repair and chromatin (Figure 1). Some of this renewed interest was the result of an increased understanding of how proteins involved in transcription interact with nucleosomes (e.g., see Meijer and Smerdon, 1999, BioEssays 21, 596). There is now convincing evidence that nucleosome modifications and rearrangements are required for efficient transcriptional processing of DNA. Since the late 70s, the Smerdon lab has focused on correlations between DNA damage, DNA repair, gene transcription and chromatin structure. Comprehensive reviews on the work done in this lab can be found in Smerdon and Conconi (1999) Prog. Nucl. Acid Res. Mol. Biol., 62:227, and Gong et al. (2005) DNA Repair 4:884.