Evidence map›Paper›PMID 28500273›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Fundamental trade-offs between information flow in single cells and cellular populations.

Ryan Suderman, John A Bachman, Adam Smith, Peter K Sorger, Eric J Deeds

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
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

58 citing papers in PubMed, 125 citations in OpenAlex.

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  5. bioRxiv : the preprint server for biology · 2024
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  19. A synthetic synthesis to explore animal evolution and development.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  20. Quantifying information of intracellular signaling: progress with machine learning.Reports on progress in physics. Physical Society (Great Britain) · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Ryan SudermanCenter for Computational Biology, University of Kansas, Lawrence, KS 66047.
John A BachmanLaboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115.
Adam SmithCenter for Computational Biology, University of Kansas, Lawrence, KS 66047.
Peter K SorgerLaboratory of Systems Pharmacology, Harvard Medical School, Boston, MA 02115.
Eric J DeedsCenter for Computational Biology, University of Kansas, Lawrence, KS 66047; deeds@ku.edu.
University of Kansas · USCenter for Systems Biology · USHarvard University · US

Funding

TRANSLATIONAL PHARMACOLOGY COREP50GM107618 · NIGMS · HARVARD MEDICAL SCHOOL · PI GOLAN, DAVID E. · 2014 to 2018
$10.8M
NIGMS NIH HHS P50 GM107618
6 · The paper itself

Abstract

Signal transduction networks allow eukaryotic cells to make decisions based on information about intracellular state and the environment. Biochemical noise significantly diminishes the fidelity of signaling: networks examined to date seem to transmit less than 1 bit of information. It is unclear how networks that control critical cell-fate decisions (e.g., cell division and apoptosis) can function with such low levels of information transfer. Here, we use theory, experiments, and numerical analysis to demonstrate an inherent trade-off between the information transferred in individual cells and the information available to control population-level responses. Noise in receptor-mediated apoptosis reduces information transfer to approximately 1 bit at the single-cell level but allows 3-4 bits of information to be transmitted at the population level. For processes such as eukaryotic chemotaxis, in which single cells are the functional unit, we find high levels of information transmission at a single-cell level. Thus, low levels of information transfer are unlikely to represent a physical limit. Instead, we propose that signaling networks exploit noise at the single-cell level to increase population-level information transfer, allowing extracellular ligands, whose levels are also subject to noise, to incrementally regulate phenotypic changes. This is particularly critical for discrete changes in fate (e.g., life vs. death) for which the key variable is the fraction of cells engaged. Our findings provide a framework for rationalizing the high levels of noise in metazoan signaling networks and have implications for the development of drugs that target these networks in the treatment of cancer and other diseases.

Indexed as

Models, BiologicalBiophysical PhenomenaCell CommunicationComputer SimulationHeLa CellsHumansInformation TheoryIon ChannelsSignal TransductionSystems BiologyTNF-Related Apoptosis-Inducing LigandIon ChannelsTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanapoptosiscellular heterogeneityinformation theorysignal transduction

Identifiers

PMID28500273
PMCPMC5465904
OpenAlexW2613783344

What OpenQuestion holds

Textmetadata
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.