Lesions in DNA: hurdles for polymerases.
Translesion synthesis (TLS) is one of the DNA damage tolerance strategies, which have evolved to enable organisms to replicate their genome despite the presence of unrepaired damage. The process of TLS has the propensity to produce mutations, a potential origin of cancer, and is therefore of medical interest. Significant progress in our understanding of TLS has come primarily from studies of the bacterium Escherichia coli, the budding yeast Saccharomyces cerevisiae and, more recently, human cells. Results from these analyses indicate that the fundamental mechanism of TLS and the proteins involved have been conserved throughout evolution from bacteria to humans.
Baynton
K
K
Institute of Medical Microbiology, Dept of Molecular Biology, Rikshospitalet, Pilestredet 32, N-0027 Oslo, Norway.
Fuchs
R P
RP
D004249:DNA Damage / Q000528:radiation effects; D004260:DNA Repair; D004259:DNA-Directed DNA Polymerase / Q000378:metabolism*; D004926:Escherichia coli / Q000235:genetics; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009713:Nucleotidyltransferases; D029701:Saccharomyces cerevisiae Proteins; D000099270:Y-Family DNA Polymerases
D004259:DNA-Directed DNA Polymerase; D005656:Fungal Proteins; D009713:Nucleotidyltransferases; D029701:Saccharomyces cerevisiae Proteins; C100951:REV1 protein, S cerevisiae; D000099270:Y-Family DNA Polymerases