Replication of damaged DNA.
DNA damage is generated continually inside cells. In order to be able to replicate past damaged bases (translesion synthesis), the cell employs a series of specialised DNA polymerases, which singly or in combination, are able to bypass many different types of damage. The polymerases have similar structural domains to classical polymerases, but they have a more open structure to allow altered bases to fit into their active sites. Although not required for replication of undamaged DNA, some at least of these polymerases are located in replication factories. Emerging evidence suggests that the polymerase switch from replicative to translesion polymerases might be mediated by post-translational modifications.
Lehmann
Alan R
AR
Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK. a.r.lehmann@sussex.ac.uk
D000818:Animals; D004249:DNA Damage / Q000502:physiology*; D004260:DNA Repair / Q000502:physiology*; D004261:DNA Replication / Q000502:physiology*; D004259:DNA-Directed DNA Polymerase / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008958:Models, Molecular; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism; D017434:Protein Structure, Tertiary / Q000235:genetics / Q000502:physiology; D034702:RNA-Binding Protein FUS / Q000235:genetics / Q000378:metabolism*; D014983:Xeroderma Pigmentosum / Q000235:genetics / Q000378:metabolism
D018809:Proliferating Cell Nuclear Antigen; D034702:RNA-Binding Protein FUS; D004259:DNA-Directed DNA Polymerase