Our DNA is subject to damaging agents, resulting in the formation of several types of damage, including single-strand and double-strand breaks, crosslink formation, and nucleobase modifications. In particular, nucleobase lesions include deamination of cytosine and 5-methylcytosine to uracil and thymine, respectively, the oxidation of guanine to 8-oxo-7,8-dihydorguanine, and the formation of abasic sites. The base excision repair (BER) pathway removes and repairs damage to nucleobases, initiated by recognition and removal of the damage by a DNA glycosylase. The resulting abasic site is then further processed in the pathway: the backbone is nicked, the deoxyribose-phosphate removed, the gap filled, and finally the backbone sealed. Though the steps of BER have been characterized on free duplex substrate, nuclear DNA is packaged into chromatin. The most basic unit of chromatin is the nucleosome core particle (NCP) consisting of ~150 bp of DNA wrapped about an octameric core of histone proteins (two copies each of H2A, H2B, H3, and H4). We seek to determine how DNA packaging affects the initiation of BER on nucleobase lesions in the context of the nucleosome core particle.<br/>

Initiation of repair of DNA nucleobase lesions in the nucleosome core particle

256th National Meeting (2018)

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