title: Proficient and accurate bypass of persistent DNA lesions by DinB DNA polymerases.
abstract: Despite nearly universal conservation through evolution, the precise function of the DinB/pol kappa branch of the Y-family of DNA polymerases has remained unclear. Recent results suggest that DinB orthologs from all domains of life proficiently bypass replication blocking lesions that may be recalcitrant to DNA repair mechanisms. Like other translesion DNA polymerases, the error frequency of DinB and its orthologs is higher than the DNA polymerases that replicate the majority of the genome. However, recent results suggest that some Y-family polymerases, including DinB and pol kappa, bypass certain types of DNA damage with greater proficiency than an undamaged template. Moreover, they do so relatively accurately. The ability to employ this mechanism to manage DNA damage may be especially important for types of DNA modification that elude repair mechanisms. For these lesions, translesion synthesis may represent a more important line of defense than for other types of DNA damage that are more easily dealt with by other more accurate mechanisms.
authors: Department of Chemistry, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
authors: Daniel F
authors: DF
authors: Jarosz
authors: Veronica G
authors: VG
authors: Godoy
authors: Graham C
authors: GC
authors: Walker
mesh_terms: D000818:Animals; D004249:DNA Damage / Q000235:genetics*; D004260:DNA Repair / Q000235:genetics*; D004261:DNA Replication / Q000235:genetics*; D004259:DNA-Directed DNA Polymerase / Q000235:genetics / Q000378:metabolism*; D019143:Evolution, Molecular; D006801:Humans; D008958:Models, Molecular; D010802:Phylogeny; D017434:Protein Structure, Tertiary / Q000502:physiology; D000099270:Y-Family DNA Polymerases
chemical_list: D004259:DNA-Directed DNA Polymerase; C404302:POLK protein, human; D000099270:Y-Family DNA Polymerases