The β Subunit Modulates Bypass and Termination at UV Lesions During in Vitro Replication with DNA Polymerase III Holoenzyme of Escherichia coli

Shavitt, O; Livneh, Zvi

doi:10.1016/s0021-9258(18)60460-0

Cited by 20 publications

(2 citation statements)

References 34 publications

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“…Van Zeeland and Filon also showed that replication forks paused only briefly at pyrimidine dimers (31). Bypass of UV lesions in vitro has also been demonstrated using E.coli DNA polymerases I (32) and III (33)(34)(35) or in the mammalian system (22,36,37). In our in vivo experiment measuring the mutation frequency of SV40 plasmid replicated in Cos-1 cells, putatively mutagenic translesion synthesis was also observed.…”

Section: Replication Elongation Proceeds On Uv-damaged Template Follo...supporting

confidence: 71%

Inhibition of initiation of simian virus 40 DNA replication during acute response of cells irradiated by ultraviolet light

Wang¹

1996

Nucleic Acids Research

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To study the mechanism by which ultraviolet (UV) light inhibits DNA replication, we examined the effects of UV 254 nm irradiation on the replication of simian virus 40 (SV40) DNA and SV40-based plasmid in monkey cells. The study was designed to determine the relative contributions made by inhibition of replication initiation and chain elongation to the immediate inhibition of DNA replication following UV irradiation. We used two-dimensional neutral-alkaline electrophoresis to examine the behaviour of replication intermediates unambiguously. Kinetic analysis using this technique showed that initiation of replication started to decline at 15 min post-irradiation. When the pulse label incorporated in SV40 replication intermediates before irradiation was chased for 1 h, most of the label was found in mature Form I and II molecules. This indicated that replication elongation took place on damaged template. We also used a transfection technique to show that heavily irradiated plasmids replicated efficiently in unirradiated transfected cells. By the transfection technique, we observed that UV irradiation of host cells dose-dependently inhibited replication of transfected non-irradiated plasmids, suggesting that the inhibition of DNA replication is due to a global change in cellular physiology induced by UV. This change was also apparent from poor staining of the chromatin by fluorescent-DNA-binding dyes immediately after UV irradiation of intact cells. We conclude that a significant fraction of chain elongation proceeds on damaged templates and DNA replication during the acute response of cells irradiated with UV is mainly controlled by the inhibition of replication initiation.

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Section: Replication Elongation Proceeds On Uv-damaged Template Follo...supporting

confidence: 71%

Inhibition of initiation of simian virus 40 DNA replication during acute response of cells irradiated by ultraviolet light

Wang¹

1996

Nucleic Acids Research

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“…These results suggest that the DNA polymerase III of E. coli and the simian DNA polymerase δ have different properties regarding the insertion of nucleotides opposite 2-OH-Ade. Alternatively, an accessory protein involved in replication may modify the fidelity of the DNA polymerases as reported (Shavitt & Livneh, 1989;O'day et al, 1992;Tadmor et al, 1992;Suzuki et al, 1994;Mozzherin et al, 1996). However, the actual reasons for these discrepancies remain to be resolved.…”

Section: Discussionmentioning

confidence: 99%

Mutations Induced by 2-Hydroxyadenine on a Shuttle Vector during Leading and Lagging Strand Syntheses in Mammalian Cells

Kamiya

Kasai

1997

Biochemistry

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An oxidatively damaged base, 2-hydroxyadenine (2-OH-Ade), was incorporated into a predetermined site of one of the strands {(+)- or (-)-strand} of the double-stranded shuttle vector, pSVK3, and the modified DNAs were transfected into simian COS-7 cells. The nucleotide sequences in which the modified base was incorporated were 5'-GTCGA*C and 5'-CTTA*AG (A* represents 2-OH-Ade). The former is the recognition site for the restriction enzyme SalI, and the latter is that for AflII. The DNAs replicated in the cells were recovered and were transfected again into Escherichia coli. The DNAs recovered from the COS-7 cells transfected with a plasmid containing 2-OH-Ade at either site of the (+)-strand (a template strand for lagging strand synthesis) formed colonies about 50%-70% as frequently as the unmodified DNA. This indicated that the base weakly blocked DNA replication during lagging strand synthesis. On the other hand, the base in the (-)-strand did not appear to affect the efficiency of leading strand synthesis in COS-7 cells. The mutation frequencies of 2-OH-Ade in COS-7 cells were 0.6%-0.1%, depending on the sequence and the strand location. Although the mutation spectra of 2-OH-Ade also differed with sequences and strands, the base elicited substitution and deletion mutations in mammalian cells, as in E. coli. These results indicate that 2-OH-Ade is mutagenic in eukaryotic cells as well as in prokaryotic cells.

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Mechanism of Induced Mutagenesis by Ultraviolet Light in Escherichia coli

Ruiz-Rubio¹

1993

Advances in Mutagenesis Research

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The β Subunit Modulates Bypass and Termination at UV Lesions During in Vitro Replication with DNA Polymerase III Holoenzyme of Escherichia coli

Cited by 20 publications

References 34 publications

Inhibition of initiation of simian virus 40 DNA replication during acute response of cells irradiated by ultraviolet light

Inhibition of initiation of simian virus 40 DNA replication during acute response of cells irradiated by ultraviolet light

Mutations Induced by 2-Hydroxyadenine on a Shuttle Vector during Leading and Lagging Strand Syntheses in Mammalian Cells

Mechanism of Induced Mutagenesis by Ultraviolet Light in Escherichia coli

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