Evidence map›Paper›PMID 29108019›Full record

ArticlePLoS biology2017

Stochastic loss and gain of symmetric divisions in the C. elegans epidermis perturbs robustness of stem cell number.

Dimitris Katsanos, Sneha L Koneru, Lamia Mestek Boukhibar, Nicola Gritti, Ritobrata Ghose, Peter J Appleford, Maria Doitsidou, Alison Woollard, Jeroen S van Zon, Richard J Poole and 1 more

Abstract read
In one paragraph

Article in PLoS biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
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  9. bioRxiv : the preprint server for biology · 2023
    Article
  10. Article
  11. Targeted DamID inScience advances · 2022
    Article
  12. Gene-Environment Interactions and Stochastic Variations in the Gero-Exposome.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021
    Article
  13. Article
  14. Article
  15. Phenotypic Robustness of Epidermal Stem Cell Number inFrontiers in cell and developmental biology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

11 authors.

Dimitris KatsanosDepartment of Life Sciences, Imperial College, London, United Kingdom.
Sneha L KoneruDepartment of Life Sciences, Imperial College, London, United Kingdom.
Lamia Mestek BoukhibarDepartment of Life Sciences, Imperial College, London, United Kingdom.
Nicola GrittiInstitute for Atomic and Molecular Physics (AMOLF), Amsterdam, The Netherlands.
Ritobrata GhoseDepartment of Life Sciences, Imperial College, London, United Kingdom.
Peter J ApplefordDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Maria DoitsidouCentre for Integrative Physiology, University of Edinburgh, Edinburgh, United Kingdom.
Alison WoollardDepartment of Biochemistry, University of Oxford, Oxford, United Kingdom.
Jeroen S van ZonInstitute for Atomic and Molecular Physics (AMOLF), Amsterdam, The Netherlands.
Richard J PooleDepartment of Cell and Developmental Biology, University College London, London, United Kingdom.
Michalis BarkoulasDepartment of Life Sciences, Imperial College, London, United Kingdom.ORCID http://orcid.org/0000-0003-1974-7668

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
Biotechnology and Biological Sciences Research Council BB/G018448/1NIH HHS P40 OD010440Wellcome Trust 207483/Z/17/Z
6 · The paper itself

Abstract

Biological systems are subject to inherent stochasticity. Nevertheless, development is remarkably robust, ensuring the consistency of key phenotypic traits such as correct cell numbers in a certain tissue. It is currently unclear which genes modulate phenotypic variability, what their relationship is to core components of developmental gene networks, and what is the developmental basis of variable phenotypes. Here, we start addressing these questions using the robust number of Caenorhabditis elegans epidermal stem cells, known as seam cells, as a readout. We employ genetics, cell lineage tracing, and single molecule imaging to show that mutations in lin-22, a Hes-related basic helix-loop-helix (bHLH) transcription factor, increase seam cell number variability. We show that the increase in phenotypic variability is due to stochastic conversion of normally symmetric cell divisions to asymmetric and vice versa during development, which affect the terminal seam cell number in opposing directions. We demonstrate that LIN-22 acts within the epidermal gene network to antagonise the Wnt signalling pathway. However, lin-22 mutants exhibit cell-to-cell variability in Wnt pathway activation, which correlates with and may drive phenotypic variability. Our study demonstrates the feasibility to study phenotypic trait variance in tractable model organisms using unbiased mutagenesis screens.

Indexed as

Cell DivisionCell LineageEpidermal CellsAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell CountCell DifferentiationCells, CulturedDNA-Binding ProteinsEpidermisGene Expression RegulationStem CellsStochastic ProcessesTranscription FactorsWnt Signaling PathwayCaenorhabditis elegans ProteinsDNA-Binding ProteinsLin-22 protein, C elegansTranscription Factors

Identifiers

PMID29108019
PMCPMC5690688

What OpenQuestion holds

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LicenceCC BY
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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.