Repair in E. coli of transforming plasmid DNA damaged by psoralen plus near-ultraviolet irradiation

Roberts, Richard J.; Strike, Peter

doi:10.1016/0167-8817(86)90063-5

Cited by 4 publications

(3 citation statements)

References 43 publications

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“…Prior to the isolation and characterization of the UvrABC subunits, several groups examined the repair of psoralen cross-links in E. coli by using a variety of biochemical and genetic approaches (36,42,43,119,134,161,217,218,280,281). They found that the repair of psoralen-cross-linked DNA required ATP, functional UvrA, UvrB, UvrC, RecA, UvrD, and DNA polymerase I, as well as the presence of multiple genomes.…”

Section: Uvr-dependent Recombinational Repairmentioning

confidence: 99%

Nucleotide excision repair in Escherichia coli.

Houten

1990

Microbiological Reviews

223

101

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Section: Uvr-dependent Recombinational Repairmentioning

confidence: 99%

Nucleotide excision repair in Escherichia coli.

Houten

1990

Microbiological Reviews

223

101

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“…This may help clarify a number of previous studies that have reached differing conclusions when characterizing repair mechanisms on transforming DNA. Strike and Roberts initially found that plasmid survival was dependent on RecBC, but curiously, it did not depend on RecA or RecF (Roberts and Strike, 1986). When normalized to an undamaged reference plasmid, we found that the survival of introduced plasmids containing UV-induced damage in recBC mutants was similar to wild-type cells and did not depend on RecA.…”

Section: Discussionmentioning

confidence: 99%

“…A series of early studies by Roberts and Strike introduced UV-irradiated plasmids and found that plasmid survival depended on UvrA and RecBC, but not on RecA or RecF, irrespective of whether a homologous plasmid was present (Roberts and Strike, 1981; Roberts and Strike, 1986; Strike and Roberts, 1982; Strike et al , 1979). In contrast, a set of more recent studies reported that survival of transforming plasmids containing bulky adducts depended on both RecA and RecF function and required the presence of a homologous plasmid (Bichara et al , 2007; Bichara et al , 2009).…”

Section: Introductionmentioning

confidence: 99%

Inefficient replication reduces RecA-mediated repair of UV-damaged plasmids introduced into competent Escherichia coli

Jeiranian

Courcelle

2012

Plasmid

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Transformation of Escherichia coli with purified plasmids containing DNA damage is frequently used as a tool to characterize repair pathways that operate on chromosomes. In this study, we used an assay that allowed us to quantify plasmid survival and to compare how efficiently various repair pathways operate on plasmid DNA introduced into cells relative to their efficiency on chromosomal DNA. We observed distinct differences between the mechanisms operating on the transforming plasmid DNA and the chromosome. An average of one UV-induced lesion was sufficient to inactivate ColE1-based plasmids introduced into nucleotide excision repair mutants, suggesting an essential role for repair on newly introduced plasmid DNA. By contrast, the absence of RecA, RecF, RecBC, RecG or RuvAB had a minimal effect on the survival of the transforming plasmid DNA containing UV-induced damage. Neither the presence of an endogenous homologous plasmid nor the induction of the SOS response enhanced the survival of transforming plasmids. Using two-dimensional agarose-gel analysis, both replication- and RecA-dependent structures that were observed on established, endogenous plasmids following UV-irradiation, failed to form on UV-irradiated plasmids introduced into E. coli. We interpret these observations to suggest that the lack of RecA-mediated survival is likely to be due to inefficient replication that occurs when plasmids are initially introduced into cells, rather than to the plasmid’s size, the absence of homologous sequences, or levels of recA expression.

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