Evidence map›Paper›PMID 23555208›Full record

ArticlePLoS computational biology2013

The fidelity of dynamic signaling by noisy biomolecular networks.

Clive G Bowsher, Margaritis Voliotis, Peter S Swain

Abstract read
In one paragraph

Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Continuous variable responses and signal gating form kinetic bases for pulsatile insulin signaling and emergence of resistance.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  2. Information transmission in a two-step cascade: interplay of activation and repression.Theory in biosciences = Theorie in den Biowissenschaften · 2021
    Article
  3. Optimal ligand discrimination by asymmetric dimerization and turnover of interferon receptors.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  9. Mathematical modeling of gonadotropin-releasing hormone signaling.Molecular and cellular endocrinology · 2017
    Review
  10. Article
  11. Article
  12. Molecular circuits for dynamic noise filtering.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  13. Article
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  18. Information transfer by leaky, heterogeneous, protein kinase signaling systems.Proceedings of the National Academy of Sciences of the United States of America · 2014
    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

3 authors.

Clive G BowsherSchool of Mathematics, University of Bristol, Bristol, United Kingdom. c.bowsher@bristol.ac.uk
Margaritis Voliotis
Peter S Swain

Funding

Medical Research Council G0701772
6 · The paper itself

Abstract

Cells live in changing, dynamic environments. To understand cellular decision-making, we must therefore understand how fluctuating inputs are processed by noisy biomolecular networks. Here we present a general methodology for analyzing the fidelity with which different statistics of a fluctuating input are represented, or encoded, in the output of a signaling system over time. We identify two orthogonal sources of error that corrupt perfect representation of the signal: dynamical error, which occurs when the network responds on average to other features of the input trajectory as well as to the signal of interest, and mechanistic error, which occurs because biochemical reactions comprising the signaling mechanism are stochastic. Trade-offs between these two errors can determine the system's fidelity. By developing mathematical approaches to derive dynamics conditional on input trajectories we can show, for example, that increased biochemical noise (mechanistic error) can improve fidelity and that both negative and positive feedback degrade fidelity, for standard models of genetic autoregulation. For a group of cells, the fidelity of the collective output exceeds that of an individual cell and negative feedback then typically becomes beneficial. We can also predict the dynamic signal for which a given system has highest fidelity and, conversely, how to modify the network design to maximize fidelity for a given dynamic signal. Our approach is general, has applications to both systems and synthetic biology, and will help underpin studies of cellular behavior in natural, dynamic environments.

Indexed as

Models, BiologicalComputational BiologyFeedback, PhysiologicalGene ExpressionSignal Transduction

Identifiers

PMID23555208
PMCPMC3610653

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.