Evidence map›Paper›PMID 26713738›Full record

ArticlePLoS computational biology2015

Capabilities and Limitations of Tissue Size Control through Passive Mechanical Forces.

Jochen Kursawe, Pavel A Brodskiy, Jeremiah J Zartman, Ruth E Baker, Alexander G Fletcher

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Choice of friction coefficient deeply affects tissue behaviour in stochastic epithelial vertex models.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  3. Article
  4. Article
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  9. Statistics of noisy growth with mechanical feedback in elastic tissues.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Are Tumor Cell Lineages Solely Shaped by Mechanical Forces?Bulletin of mathematical biology · 2017
    Article
  15. Article
  16. Mechanocellular models of epithelial morphogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  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

5 authors at 3 institutions in 2 countries.

Jochen KursaweMathematical Institute, University of Oxford, Oxford, United Kingdom.
Pavel A BrodskiyDepartment of Chemical and Biomolecular Engineering, University of Notre Dame, Notre Dame, Indiana, United States of America.
Jeremiah J ZartmanDepartment of Chemical and Biomolecular Engineering, University of Notre Dame, Notre Dame, Indiana, United States of America.
Ruth E BakerMathematical Institute, University of Oxford, Oxford, United Kingdom.
Alexander G FletcherMathematical Institute, University of Oxford, Oxford, United Kingdom.
University of Notre Dame · USUniversity of Oxford · GBUniversity of Sheffield · GB

Funding

Multiscale modeling and empirical study of a mechanism limiting blood clot growthU01HL116330 · NHLBI · UNIVERSITY OF NOTRE DAME · PI ALBER, MARK · 2014 to 2018
$3.5M
NHLBI NIH HHS U01 HL116330NHLBI NIH HHS UO1 HL116330
6 · The paper itself

Abstract

Embryogenesis is an extraordinarily robust process, exhibiting the ability to control tissue size and repair patterning defects in the face of environmental and genetic perturbations. The size and shape of a developing tissue is a function of the number and size of its constituent cells as well as their geometric packing. How these cellular properties are coordinated at the tissue level to ensure developmental robustness remains a mystery; understanding this process requires studying multiple concurrent processes that make up morphogenesis, including the spatial patterning of cell fates and apoptosis, as well as cell intercalations. In this work, we develop a computational model that aims to understand aspects of the robust pattern repair mechanisms of the Drosophila embryonic epidermal tissues. Size control in this system has previously been shown to rely on the regulation of apoptosis rather than proliferation; however, to date little work has been done to understand the role of cellular mechanics in this process. We employ a vertex model of an embryonic segment to test hypotheses about the emergence of this size control. Comparing the model to previously published data across wild type and genetic perturbations, we show that passive mechanical forces suffice to explain the observed size control in the posterior (P) compartment of a segment. However, observed asymmetries in cell death frequencies across the segment are demonstrated to require patterning of cellular properties in the model. Finally, we show that distinct forms of mechanical regulation in the model may be distinguished by differences in cell shapes in the P compartment, as quantified through experimentally accessible summary statistics, as well as by the tissue recoil after laser ablation experiments.

Indexed as

Models, BiologicalAnimalsBiomechanical PhenomenaCell DeathCell ProliferationCell ShapeComputational BiologyDrosophilaEmbryonic Development

Identifiers

PMID26713738
PMCPMC4703071
OpenAlexW2949304048

What OpenQuestion holds

Textmetadata
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.