Abstract
Using strains of Escherichia coli K-12 that are deleted for the polA gene, we have reexamined the role of DNA polymerase I (encoded by polA) in postreplication repair after UV irradiation. The polA deletion (in contrast to the polA1 mutation) made uvrA cells very sensitive to UV radiation; the UV radiation sensitivity of a uvrA delta polA strain was about the same as that of a uvrA recF strain, a strain known to be grossly deficient in postreplication repair. The delta polA mutation interacted synergistically with a recF mutation in UV radiation sensitization, suggesting that the polA gene functions in pathways of postreplication repair that are largely independent of the recF gene. When compared to a uvrA strain, a uvrA delta polA strain was deficient in the repair of DNA daughter strand gaps, but not as deficient as a uvrA recF strain. Introduction of the delta polA mutation into uvrA recF cells made them deficient in the repair of DNA double-strand breaks after UV irradiation. The UV radiation sensitivity of a uvrA polA546(Ts) strain (defective in the 5'----3' exonuclease of DNA polymerase I) determined at the restrictive temperature was very close to that of a uvrA delta polA strain. These results suggest a major role for the 5'----3' exonuclease activity of DNA polymerase I in postreplication repair, in the repair of both DNA daughter strand gaps and double-strand breaks.
MeSH Terms
Chloramphenicol/pharmacology
DNA Polymerase I/metabolism
DNA Repair
DNA Replication
DNA, Bacterial/drug effects,genetics,metabolism,radiation effects
Escherichia coli/drug effects,enzymology,genetics,radiation effects
Genes, Bacterial
Mutation
Ultraviolet Rays
Chemicals
DNA, Bacterial
Chloramphenicol
DNA Polymerase I
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Sharma R C
Department of Therapeutic Radiology, Stanford University School of Medicine, California 94305.
Smith K C
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