Effect of Mutations in lig and polA on UV-Induced Strand Cutting in a uvrC Strain of Escherichia coli

Seeberg, Erling; Wd, Rupp

doi:10.1007/978-1-4684-2898-8_3

Cited by 19 publications

(16 citation statements)

References 2 publications

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“…The extra ligase would not be expected to have any effect on uvr-J, which is defective in the specific UV endonuclease (13). This hypothesis is in accord with the report that ligase in E. coli can seal the nicks made by the UV endonuclease * before the dimers have been released (11). In wild-type E. coli, the fact that extra ligase does not change UV sensitivity l (1) may be because the uvrC+ product prevents sealing of 10 20O…”

supporting

confidence: 63%

Plasmid containing a DNA ligase gene from Haemophilus influenzae

McCarthy¹,

Griffin²,

Setlow³

1984

J Bacteriol

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supporting

confidence: 63%

Plasmid containing a DNA ligase gene from Haemophilus influenzae

McCarthy¹,

Griffin²,

Setlow³

1984

J Bacteriol

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“…Although studies of UV-induced DNA strand breakage in the mutants have consistently shown that uvrA+ and uvrB+ gene functions are essential for the endonucleolytic event initiating repair (10,17,22), conflicting reports have been published with respect to the role of the uvrC' gene in the same process. Some reports indicate that the uvrC' gene function is involved in the actual incision reaction (2,17,18,22), whereas others point to a role for the uvrC' function in a succeeding preex'cision step (10,19,20). In view of this confusion, we reexamined the role of the uvrC function in the incision of UV-irradiated DNA, both in vitro and in vivo.…”

mentioning

confidence: 96%

Impaired incision of ultraviolet-irradiated deoxyribonucleic acid in uvrC mutants of Escherichia coli

Seeberg¹,

Rupp²,

Strike³

1980

J Bacteriol

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The production of single-strand breaks in the deoxyribonucleic acid of irradiated uvrC mutants of Escherichia coli K-12 was studied both in vivo and in vitro. In vivo, uvrC mutants displayed a slow accumulation of breaks after irradiation, and in this respect appeared different from uvrA mutants, in which very few breaks could be detected. The breakage observed in uvrC mutants differed from that observed in wild-type strains in both the slow rate of break accumulation and the very limited dose response. The behavior of the uvrC lig-7(Ts) double mutant was shown not to be consistent with the suggestion of ligase reversal as the explanation for the lower rate and limited dose response of break formation observed in ultraviolet-irradiated uvrC mutants in vivo. Rather, there appeared to be a real defect in incision. In toluene-treated cells, we studied the effect of the ligase inhibitor nicotinamide mononucleotide on strand incision. Whereas uvrC mutants displayed more strand breakage in the presence of this inhibitor, the same amount of breakage was seen in uvrA mutants, and as such the breakage could be judged as not due to the main excision repair pathway. Experiments using a cell-free system comprising the partially purified uvr+ gene products demonstrated clearly that there is a requirement for the uvrC+ gene product for strand incision. We suggest that in vivo in the absence of the uvrC+ gene product, a partial analog of this protein may allow some abnormal incision.

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“…However, the extent of incision is still limited compared to wild-type strains, and does not exceed the level normally seen in uvrC cells after prolonged incubation. In these respects, the behaviour of the uvrC34 lexA5l strain is very similar to that of a uvrC34 lig-7(Ts) strain, provided the latter has been incubated at the non-permissive temperature for at least 60 min (Seeberg & Rupp, 1975). This similarity might well be a reflection of the effective induction of SOS functions by ligase inactivation (Morse & Pauling, 1975).…”

Section: Sos Dependence Of Incision In Uurc34 Mutantsmentioning

confidence: 78%

“…If ligase is inactivated in intact cells by the introduction of a lig-7(Ts) mutation and preincubation at the non-permissive temperature, the initial rate (but not the final level) of postirradiation incision is increased in uvrC mutants (Seeberg & Rupp, 1975 (Seeberg et al, 1980). Ligase inactivation leads to efficient induction of the SOS regulon (Morse & Pauling, 1975).…”

Section: Introductionmentioning

confidence: 99%

A Transposon Insertion in the Escherichia coli uvrC Gene; UvrC Protein is Absolutely Required for the Incision Step in Excision Repair

Walters

Wilbraham²,

Strike³

et al. 1988

Microbiology

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~~The formation of single-stranded breaks in DNA following UV irradiation is assessed in uvrC34 mutants. By altering the SOS DNA-repair system, either by additional mutations or by using drugs affecting transcription or translation, it is shown that such single-stranded breaks require one or more DN A-damage-inducible functions. A UV-sensitive strain is characterized as carrying a TnZO insertion into the uvrC gene. The absence of post-irradiation incision in this strain demonstrates that uvrC function is absolutely required in vivo for the incision stage of excision repair, and suggests that other uvrC mutants are 'leaky'.

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Effect of Mutations in lig and polA on UV-Induced Strand Cutting in a uvrC Strain of Escherichia coli

Cited by 19 publications

References 2 publications

Plasmid containing a DNA ligase gene from Haemophilus influenzae

Plasmid containing a DNA ligase gene from Haemophilus influenzae

Impaired incision of ultraviolet-irradiated deoxyribonucleic acid in uvrC mutants of Escherichia coli

A Transposon Insertion in the Escherichia coli uvrC Gene; UvrC Protein is Absolutely Required for the Incision Step in Excision Repair

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