Evidence map›Paper›PMID 31466698›Full record

ArticleBiophysical journal2019

A Quantitative Model Explains Single-Cell Dynamics of the Adaptive Response in Escherichia coli.

Stephan Uphoff

Abstract read
In one paragraph

Article in Biophysical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Stephan UphoffDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom. Electronic address: stephan.uphoff@bioch.ox.ac.uk.

Funding

Wellcome TrustWellcome Trust 101636/Z/13/ZWellcome Trust 206159/Z/17/BWellcome Trust 206159/Z/17/Z
6 · The paper itself

Abstract

DNA damage caused by alkylating chemicals induces an adaptive response in Escherichia coli that increases the tolerance of cells to further damage. Signaling of the response occurs through irreversible methylation of the Ada protein, which acts as a DNA repair protein and damage sensor. Methylated Ada induces its own gene expression through a positive feedback loop. However, random fluctuations in the abundance of Ada jeopardize the reliability of the induction signal. I developed a quantitative model to test how gene expression noise and feedback amplification affect the fidelity of the adaptive response. A remarkably simple model accurately reproduced experimental observations from single-cell measurements of gene expression dynamics in a microfluidic device. Stochastic simulations showed that delays in the adaptive response are a direct consequence of the very low number of Ada molecules present to signal DNA damage. For cells that have zero copies of Ada, response activation becomes a memoryless process that is dictated by an exponential waiting time distribution between basal Ada expression events. Experiments also confirmed the model prediction that the strength of the adaptive response drops with an increasing growth rate of cells.

Indexed as

Adaptation, PhysiologicalModels, BiologicalSingle-Cell AnalysisDNA DamageEscherichia coliGene Expression RegulationStochastic Processes

Identifiers

PMID31466698
PMCPMC6818145

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.