Analysis of DNA damage-induced histone H3 acetylation during nucleotide excision repair of Schizosaccharomyces pombe

Abstract

Nucleotide excision repair (NER) is a robust defense mechanism to remove UV-damaged lesions in DNA. In Saccharomyces cerevisiae, the Rad7p/Rad16p NER complex mediates histone H3 acetylation (H3Ac), which results in chromatin remodeling required for efficient NER. UV-induced H3Ac occurs via Gcn5p histone acetyltranferase (HAT). Although Schizosaccharomyces pombe possesses NER genes homologous to those of S. cerevisiae, the NER pathway has not been extensively investigated. To examine the role of chromatin remodeling in S. pombe NER, we measured H3Ac of the whole genome after UV irradiation. The effect of HAT inhibitors CPTH2 and MB-3 on the repair activity of UV damage was also measured. Gcn5p and Ada2p are components of a SAGA chromatin remodeling complex. We examined the involvement of ada2 in NER and UV-dependent H3Ac. Unlike S. cerevisiase, H3Ac did not play a crucial role in NER in S. pombe cells under our experimental conditions. These results imply differences in the initial step of NER between S. cerevisiase and S. pombe.