Abstract
To counteract the deleterious effects of genotoxic injury, cells have set up a sophisticated network of DNA repair pathways. We show that Gal4-VP16 and RAR transcriptional activators stimulate nucleotide excision repair (NER). This DNA repair activation is not coupled to transcription since it occurs in Cockayne syndrome cells (which are transcription-coupled repair deficient) and is observed in vitro in the presence of alpha-amanitin and in the absence of the basal transcription factors. Using a reconstituted dual incision assay, we also show that binding of activators to their cognate sequences induces a local chromatin remodeling mediated by ATP-driven chromatin remodeling and acetyltransferase activities to facilitate DNA repair.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Base Sequence
-
Binding Sites
-
Cell Line, Transformed
-
DNA / chemistry
-
DNA / metabolism*
-
DNA Repair / physiology*
-
DNA-Binding Proteins
-
Herpes Simplex Virus Protein Vmw65 / metabolism
-
Humans
-
Oligodeoxyribonucleotides / chemistry
-
Receptors, Retinoic Acid / metabolism
-
Recombinant Fusion Proteins / metabolism
-
Restriction Mapping
-
Saccharomyces cerevisiae Proteins / metabolism
-
Simian virus 40 / genetics
-
Templates, Genetic
-
Trans-Activators / metabolism*
-
Transcription Factors / metabolism
-
Transcription, Genetic*
-
Transfection
Substances
-
DNA-Binding Proteins
-
GAL4 protein, S cerevisiae
-
Herpes Simplex Virus Protein Vmw65
-
Oligodeoxyribonucleotides
-
Receptors, Retinoic Acid
-
Recombinant Fusion Proteins
-
Saccharomyces cerevisiae Proteins
-
Trans-Activators
-
Transcription Factors
-
DNA