MULTIPLE PATHWAYS OF DNA REPAIR IN BACTERIA AND THEIR ROLES IN MUTAGENESIS*

Abstract

Abstract— In bacteria, three processes of DNA repair are known: photoreactivation, excision repair, and postreplication repair. Photoreactivation, the enzymatic splitting of cyclobutyl pyrimidine dimers in situ, is mediated by exposure of the enzyme‐dimer complex to near‐UV and visible light. This repair process appears to be error free. The excision repair of UV‐induced DNA base damage has been divided into two major pathways on the basis of both physiological requirements and genetic control. The major pathway requires a functional pol A gene, does not require complete growth medium. and appears to be largely error‐free and to produce short patches during repair. The second pathway requires complete growth medium and functional recA, recB, recC, lexA, uvrD, and polC genes, and appears to be mutagenic and to produce long patches during repair. There exists a second type of excision repair in which the modified base is removed by an N‐glycosidase, and the chain is then nicked by an apurinic (apyrimidinic) acid endonuclease. Subsequent events are presumed to be similar to the above excision repair process. The postreplication repair system has been divided into at least four separate pathways. Three of these are dependent upon functional recB, lexA, and uvrD genes, respectively, and appear to be error free. A fourth pathway depends upon the above gene products, but is blocked by postirradiation treatment with chloramphenicol, and may be the UV‐inducible, errorprone, mutagenic pathway of repair (“SOS repair”). A possible fifth pathway depends upon a functional recF gene, and is independent of the recB+‐dependent pathway. Mutagenesis appears to be the result of error‐prone DNA repair, and there is growing evidence that carcinogenesis is also the result of error‐prone DNA repair.