Turnover in bacterial DNA containing thymine or 5-bromouracil

Grivell, Anthony R.; Grivell, Marlene B.; Hanawalt, Philip C.

doi:10.1016/s0022-2836(75)80110-0

Cited by 31 publications

(8 citation statements)

References 33 publications

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“…Our results demonstrate that NER, and the Y-family polymerase PolY1, increase transcription-dependent mutagenesis in lagging-strand genes, suggesting that these regions are particularly susceptible to DNA lesions. Consistent with our findings, the classic observation that a significant amount of DNA turnover (up to 0.02% of the genome) occurs in cells unexposed to exogenous DNA damage hints at repair of basal DNA damage (84). Although determining the exact chemical structure of the predicted DNA lesions at regions of conflict between replication and transcription is beyond the scope of this study, recent reports, as well as classic publications, suggest several different cellular sources of damage potentially leading to NER.…”

Section: Discussionsupporting

confidence: 92%

An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis

Million-Weaver¹,

Samadpour²,

Moreno-Habel³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

128

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We previously reported that lagging-strand genes accumulate mutations faster than those encoded on the leading strand in Bacillus subtilis. Although we proposed that orientation-specific encounters between replication and transcription underlie this phenomenon, the mechanism leading to the increased mutagenesis of lagging-strand genes remained unknown. Here, we report that the transcription-dependent and orientation-specific differences in mutation rates of genes require the B. subtilis Y-family polymerase, PolY1 (yqjH). We find that without PolY1, association of the replicative helicase, DnaC, and the recombination protein, RecA, with lagging-strand genes increases in a transcription-dependent manner. These data suggest that PolY1 promotes efficient replisome progression through lagging-strand genes, thereby reducing potentially detrimental breaks and single-stranded DNA at these loci. Y-family polymerases can alleviate potential obstacles to replisome progression by facilitating DNA lesion bypass, extension of D-loops, or excision repair. We find that the nucleotide excision repair (NER) proteins UvrA, UvrB, and UvrC, but not RecA, are required for transcription-dependent asymmetry in mutation rates of genes in the two orientations. Furthermore, we find that the transcription-coupling repair factor Mfd functions in the same pathway as PolY1 and is also required for increased mutagenesis of laggingstrand genes. Experimental and SNP analyses of B. subtilis genomes show mutational footprints consistent with these findings. We propose that the interplay between replication and transcription increases lesion susceptibility of, specifically, lagging-strand genes, activating an Mfd-dependent error-prone NER mechanism. We propose that this process, at least partially, underlies the accelerated evolution of lagging-strand genes.replication conflicts | transcription orientation | Y-family polymerases | excision repair | TCR

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Section: Discussionsupporting

confidence: 92%

An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis

Million-Weaver¹,

Samadpour²,

Moreno-Habel³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

128

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“…In an early approach to answer this question we simply measured the background level of repair replication or 'DNA turnover' in E. coli which had not been exposed to any DNA damaging agent. Using the 5-bromouracil density-labeling protocol we detected a low level of repair replication (Couch and Hanawalt, 1967) and this was quantified in later studies at the level of roughly 0.02% of the nucleotides replaced per hour (Grivell et al, 1975). Curiously, we found that much of this 'turnover' was dependent upon transcription.…”

Section: Gratuitous Ner In Undamaged Dna?mentioning

confidence: 78%

Subpathways of nucleotide excision repair and their regulation

2002

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“…While extensive DNA replication does not occur under these conditions, a number of early studies showed that some DNA is synthesized in starving E. coli cells, a necessary precursor if the DNA damage is to lead to mutations (53, 99, 103, 174, 213, 214). In fact, the phenomenon of stationary-phase mutation was first described in the late 1960s and attributed to repair DNA synthesis (98).…”

Section: Dna Synthesis In Non-dividing Cellsmentioning

confidence: 99%

Stress-Induced Mutagenesis

Williams

Foster

2012

EcoSal Plus

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Early research on the origins and mechanisms of mutation led to the establishment of the dogma that, in the absence of external forces, spontaneous mutation rates are constant. However, recent results from a variety of experimental systems suggest that mutation rates can increase in response to selective pressures. This chapter summarizes data demonstrating that,under stressful conditions, Escherichia coli and Salmonella can increase the likelihood of beneficial mutations by modulating their potential for genetic change.Several experimental systems used to study stress-induced mutagenesis are discussed, with special emphasison the Foster-Cairns system for "adaptive mutation" in E. coli and Salmonella . Examples from other model systems are given to illustrate that stress-induced mutagenesis is a natural and general phenomenon that is not confined to enteric bacteria. Finally, some of the controversy in the field of stress-induced mutagenesis is summarized and discussed, and a perspective on the current state of the field is provided.

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Turnover in bacterial DNA containing thymine or 5-bromouracil

Cited by 31 publications

References 33 publications

An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis

An underlying mechanism for the increased mutagenesis of lagging-strand genes in Bacillus subtilis

Subpathways of nucleotide excision repair and their regulation

Stress-Induced Mutagenesis

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