APE1-dependent base excision repair of DNA photodimers in human cells

0576839 - ÚMG 2024 RIV US eng J - Článek v odborném periodiku
Gautam, A. - Fawcett, H. - Burdová, Kamila - Brazina, J. - Caldecott, K. W.
APE1-dependent base excision repair of DNA photodimers in human cells.
Molecular Cell. Roč. 83, č. 20 (2023), s. 3669-3678.e7. ISSN 1097-2765. E-ISSN 1097-4164
Institucionální podpora: RVO:68378050
Klíčová slova: base excision repair * nucleotide excision repair * parp1 * photoproducts * single-strand break repair
Obor OECD: Biochemistry and molecular biology
Impakt faktor: 16, rok: 2022
Způsob publikování: Open access
https://www.sciencedirect.com/science/article/pii/S1097276523007359?pes=vor

UV irradiation induces ,,bulky,, DNA photodimers such as (6-4)-photoproducts and cyclobutane pyrimidine dimers that are removed by nucleotide excision repair, a complex process defective in the sunlight-sensitive and cancer-prone disease xeroderma pigmentosum. Some bacteria and lower eukaryotes can also repair photodimers by enzymatically simpler mechanisms, but such pathways have not been reported in normal human cells. Here, we have identified such a mechanism. We show that normal human cells can employ a DNA base excision repair process involving NTH1, APE1, PARP1, XRCC1, and FEN1 to rapidly remove a subset of photodimers at early times following UVC irradiation. Loss of these proteins slows the early rate of repair of photodimers in normal cells, ablates their residual repair in xeroderma pigmentosum cells, and increases UVC sensitivity ∼2-fold. These data reveal that human cells can excise photodimers using a long-patch base excision repair process that functions additively but independently of nucleotide excision repair.
Trvalý link: https://hdl.handle.net/11104/0346237