Suppression of the E. coli SOS response by dNTP pool changes

Masłowska, Katarzyna H.; Makiela‐Dzbenska, Karolina; Fijałkowska, Iwona J.; Schaaper, Roel M.

doi:10.1093/nar/gkv217

Cited by 19 publications

(12 citation statements)

References 75 publications

(114 reference statements)

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“…Remarkably, in the presence of the ndk or dcd deficiency (that changes the levels of particular nucleotides) a near complete shutdown was observed of the entire SOS system. The effect is mediated most likely through the direct role of the dNTPs in the activation of the RecA protein coprotease activity facilitating the LexA repressor cleavage (Maslowska et al, ).…”

Section: Role Of Dntp Pools In Sos Inductionmentioning

confidence: 99%

The SOS system: A complex and tightly regulated response to DNA damage

Masłowska

Makiela‐Dzbenska

Fijałkowska

2019

Environ and Mol Mutagen

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324

212

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Genomes of all living organisms are constantly threatened by endogenous and exogenous agents that challenge the chemical integrity of DNA. Most bacteria have evolved a coordinated response to DNA damage. In Escherichia coli , this inducible system is termed the SOS response. The SOS global regulatory network consists of multiple factors promoting the integrity of DNA as well as error‐prone factors allowing for survival and continuous replication upon extensive DNA damage at the cost of elevated mutagenesis. Due to its mutagenic potential, the SOS response is subject to elaborate regulatory control involving not only transcriptional derepression, but also post‐translational activation, and inhibition. This review summarizes current knowledge about the molecular mechanism of the SOS response induction and progression and its consequences for genome stability. Environ. Mol. Mutagen. 60:368–384, 2019. © 2018 The Authors. Environmental and Molecular Mutagenesis published by Wiley Periodicals, Inc. on behalf of Environmental Mutagen Society.

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Section: Role Of Dntp Pools In Sos Inductionmentioning

confidence: 99%

The SOS system: A complex and tightly regulated response to DNA damage

Masłowska

Makiela‐Dzbenska

Fijałkowska

2019

Environ and Mol Mutagen

Self Cite

324

212

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“…To test this hypothesis we performed a MA experiment with a mutL ndk double mutant strain. The ndk gene encodes nucleoside diphosphate kinase, and, in its absence, the cellular concentration of dCTP increases at least twofold (Schaaper and Mathews 2013) and as much as 12-fold (Maslowska et al 2015). Relative to the MMR defective strains, loss of Ndk increased the BPS rate 5.4 6 0.1-fold overall, with the largest increases in A:T to G:C transitions (6.7 6 0.09-fold), and A:T to C:G transversions (25.6 6 0.6-fold) (values are means 6 95%CLs).…”

Section: Mononucleotide Runs Are Hotspots For Bpssmentioning

confidence: 99%

Determinants of Base-Pair Substitution Patterns Revealed by Whole-Genome Sequencing of DNA Mismatch Repair DefectiveEscherichia coli

et al. 2018

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Mismatch repair (MMR) is a major contributor to replication fidelity, but its impact varies with sequence context and the nature of the mismatch. Mutation accumulation experiments followed by whole-genome sequencing of MMR-defective strains yielded ≈30,000 base-pair substitutions (BPSs), revealing mutational patterns across the entire chromosome. The BPS spectrum was dominated by A:T to G:C transitions, which occurred predominantly at the center base of 5'NC3'+5'GN3' triplets. Surprisingly, growth on minimal medium or at low temperature attenuated these mutations. Mononucleotide runs were also hotspots for BPSs, and the rate at which these occurred increased with run length. Comparison with ≈2000 BPSs accumulated in MMR-proficient strains revealed that both kinds of hotspots appeared in the wild-type spectrum and so are likely to be sites of frequent replication errors. In MMR-defective strains transitions were strand biased, occurring twice as often when A and C rather than T and G were on the lagging-strand template. Loss of nucleotide diphosphate kinase increases the cellular concentration of dCTP, which resulted in increased rates of mutations due to misinsertion of C opposite A and T. In an double mutant strain, these mutations were more frequent when the template A and T were on the leading strand, suggesting that lagging-strand synthesis was more error-prone, or less well corrected by proofreading, than was leading strand synthesis.

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“…For E. coli, nucleotides were extracted as described (Maslowska et al 2015). The resulting nucleotide samples were then analyzed using the HPLC-UV profiling method mentioned above.…”

Section: Nucleotide Profiling By Hplc-uvmentioning

confidence: 99%

Nucleotide levels regulate germline proliferation through modulating GLP-1/Notch signaling inC. elegans

et al. 2016

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Animals alter their reproductive programs to accommodate changes in nutrient availability, yet the connections between known nutrient-sensing systems and reproductive programs are underexplored, and whether there is a mechanism that senses nucleotide levels to coordinate germline proliferation is unknown. We established a model system in which nucleotide metabolism is perturbed in both the nematode Caenorhabditis elegans (cytidine deaminases) and its food (Escherichia coli); when fed food with a low uridine/thymidine (U/T) level, germline proliferation is arrested. We provide evidence that this impact of U/T level on the germline is critically mediated by GLP-1/Notch and MPK-1/MAPK, known to regulate germline mitotic proliferation. This germline defect is suppressed by hyperactivation of glp-1 or disruption of genes downstream from glp-1 to promote meiosis but not by activation of the IIS or TORC1 pathways. Moreover, GLP-1 expression is post-transcriptionally modulated by U/T levels. Our results reveal a previously unknown nucleotide-sensing mechanism for controlling reproductivity.

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Suppression of the E. coli SOS response by dNTP pool changes

Cited by 19 publications

References 75 publications

The SOS system: A complex and tightly regulated response to DNA damage

The SOS system: A complex and tightly regulated response to DNA damage

Determinants of Base-Pair Substitution Patterns Revealed by Whole-Genome Sequencing of DNA Mismatch Repair DefectiveEscherichia coli

Nucleotide levels regulate germline proliferation through modulating GLP-1/Notch signaling inC. elegans

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