Following the RAD6 pathway.
Errol Friedberg suggested that I write a biographical account of the work carried out in my lab for the Historical Reflections section of the DNA Repair. Although I started out studying meiotic recombination, I have spent much of the last four and a half decades focused on trying to understand the mechanism underlying induced mutagenesis, which led me into what was eventually called DNA damage tolerance, the process that facilitates the resumption of replication when replicases are stalled at sites of DNA template damage. The following account highlights some of our work that contributed to an understanding of the mechanisms underlying these activities, carried out by the RAD6 pathway, my main preoccupation over this period.
Lawrence
Christopher W
CW
Department of Biochemistry and Biophysics, University of Rochester School of Medicine and Dentistry, 602 Elmwood Avenue, Rochester, NY 14642, United States. christopher_lawrence@urmc.rochester.edu
D004249:DNA Damage; D004260:DNA Repair; D004261:DNA Replication; D015966:Gene Expression Regulation, Fungal; D016296:Mutagenesis; D011995:Recombination, Genetic; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000254:growth & development; D029701:Saccharomyces cerevisiae Proteins / Q000235:genetics*; D015398:Signal Transduction; D044763:Ubiquitin-Conjugating Enzymes / Q000235:genetics*
D029701:Saccharomyces cerevisiae Proteins; C471606:RAD6 protein, S cerevisiae; D044763:Ubiquitin-Conjugating Enzymes