Events associated with DNA replication disruption are not observed in hydrogen peroxide-treated <i>Escherichia coli</i>

Hoff, Chettar A.; Schmidt, Sierra S.; Hackert, Brandy J.; Worley, Travis K; Courcelle, Justin; Courcelle, Charmain T.

doi:10.1093/g3journal/jkab044

Cited by 3 publications

(2 citation statements)

References 101 publications

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“…Together, these results demonstrate that the induction of scavenging enzymes effectively protects cells against H 2 O 2 present in their environment, reducing the formation of oxidative DNA damage down to the basal level within 30 min of continuous oxidative stress. This explains observations from genetic studies that the deletion of BER and NER enzymes does not sensitise cells to killing by H 2 O 2 (Hoff et al , 2021 ).…”

Section: Resultsmentioning

confidence: 84%

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

2022

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Understanding the interplay between phenotypic and genetic adaptation is a focus of evolutionary biology. In bacteria, the oxidative stress response prevents mutagenesis by reactive oxygen species (ROS). We hypothesise that the stress response dynamics can therefore affect the timing of the mutation supply that fuels genetic adaptation to oxidative stress. We uncover that sudden hydrogen peroxide stress causes a burst of mutations. By developing single‐molecule and single‐cell microscopy methods, we determine how these mutation dynamics arise from phenotypic adaptation mechanisms. H2O2 signalling by the transcription factor OxyR rapidly induces ROS‐scavenging enzymes. However, an adaptation delay leaves cells vulnerable to the mutagenic and toxic effects of hydroxyl radicals generated by the Fenton reaction. Resulting DNA damage is counteracted by a spike in DNA repair activities during the adaptation delay. Absence of a mutation burst in cells with prior stress exposure or constitutive OxyR activation shows that the timing of phenotypic adaptation directly controls stress‐induced mutagenesis. Similar observations for alkylation stress show that mutation bursts are a general phenomenon associated with adaptation delays.

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Section: Resultsmentioning

confidence: 84%

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

2022

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“…Together, these results demonstrate that the induction of the oxidative stress response effectively protects cells against H2O2 present in their environment, reducing the formation of oxidative DNA damage down to the basal level within 30 min of continuous oxidative stress. This explains observations from genetic studies that deletion of BER and NER enzymes does not sensitise cells to killing by H2O2 (Hoff et al, 2021).…”

Section: Dna Repair Dynamics During Oxidative Stressmentioning

confidence: 81%

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

Lagage

Chen

Uphoff

2022

Preprint

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Understanding the interplay between phenotypic plasticity and genetic adaptation is a long-standing focus of evolutionary biology. In bacteria, the oxidative stress response limits the formation of mutagenic reactive oxygen species (ROS) under diverse stress conditions. This suggests that the dynamics of the oxidative stress response are closely tied to the timing of the mutation supply that fuels genetic adaptation to stress. Here, we explored how mutation rates change in real-time in Escherichia coli cells during continuous hydrogen peroxide treatment in microfluidic channels. By visualising nascent DNA replication errors, we uncovered that sudden oxidative stress causes a burst of mutations. We developed a range of single-molecule and single-cell microscopy assays to determine how these mutation dynamics arise from phenotypic adaptation mechanisms. Signalling of peroxide stress by the transcription factor OxyR rapidly induces ROS scavenging enzymes. However, an adaptation delay leaves cells vulnerable to the mutagenic and toxic effects of hydroxyl radicals generated by the Fenton reaction. Resulting DNA damage is counteracted by a spike in DNA repair activities during the adaptation delay. Prior stress exposure or constitutive OxyR induction allowed cells to avoid the burst of mutations. Similar observations for alkylation stress show that mutation bursts are a general phenomenon associated with adaptation delays.

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Manganese transporters regulate the resumption of replication in hydrogen peroxide-stressed Escherichia coli

Wang,

Courcelle,

Coltman

et al. 2023

Biometals

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Events associated with DNA replication disruption are not observed in hydrogen peroxide-treated Escherichia coli

Cited by 3 publications

References 101 publications

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

Adaptation delay causes a burst of mutations in bacteria responding to oxidative stress

Manganese transporters regulate the resumption of replication in hydrogen peroxide-stressed Escherichia coli

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