Abstract:
:OGG1 initiated base excision repair (BER) is the major pathway for repair of oxidative DNA base damage 8-oxoguanine (8-oxoG). Here, we report that RECQL4 DNA helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically and functionally interacts with OGG1. RECQL4 promotes catalytic activity of OGG1 and RECQL4 deficiency results in defective 8-oxoG repair and increased genomic 8-oxoG. Furthermore, we show that acute oxidative stress leads to increased RECQL4 acetylation and its interaction with OGG1. The NAD+-dependent protein SIRT1 deacetylates RECQL4 in vitro and in cells thereby controlling the interaction between OGG1 and RECQL4 after DNA repair and maintaining RECQL4 in a low acetylated state. Collectively, we find that RECQL4 is involved in 8-oxoG repair through interaction with OGG1, and that SIRT1 indirectly modulates BER of 8-oxoG by controlling RECQL4-OGG1 interaction.
journal_name
Nucleic Acids Resjournal_title
Nucleic acids researchauthors
Duan S,Han X,Akbari M,Croteau DL,Rasmussen LJ,Bohr VAdoi
10.1093/nar/gkaa392subject
Has Abstractpub_date
2020-07-09 00:00:00pages
6530-6546issue
12eissn
0305-1048issn
1362-4962pii
5841135journal_volume
48pub_type
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