Controlling the efficiency of excision repair

摘要: The early studies are recounted, that led to the discovery of ubiquitous process DNA excision repair, followed by a review pathways transcription-coupled repair (TCR) and global genomic nucleotide (GGR). Repair replication damaged in UV-irradiated bacteria was discovered through use 5-bromouracil density-label newly synthesized DNA. This assay then used human cells validate phenomenon unscheduled synthesis as measure elucidate first example disorder, xeroderma pigmentosum. Features TCR pathway (that is defective Cockayne syndrome (CS)) include possibility "gratuitous TCR" at transcription pause sites undamaged GGR shown be controlled SOS stress response E. coli activated product p53 tumor suppressor gene cells. These regulatory systems particularly affect efficiency predominant UV-induced photoproduct, cyclobutane pyrimidine dimer, well chemical carcinogen adducts, such benzo(a)pyrene diol-epoxide. Rodent (typically lacking p53-controlled pathway) virus infected (in which function abrogated) unable carry out efficient some lesions. Therefore, caution should exercised interpretation results from for risk assessment genetic toxicology. Many problems remain solved, including mechanism scanning lesions subcellular localization factories. Also there persisting questions regarding multiple options recombination, translesion when forks encounter template That where field began four decades ago with on recovery bacteria.