Evidence map›Paper›PMID 24855951›Full record

ArticleCell2014

Compensatory flux changes within an endocytic trafficking network maintain thermal robustness of Notch signaling.

Hideyuki Shimizu, Simon A Woodcock, Marian B Wilkin, Barbora Trubenová, Nicholas A M Monk, Martin Baron

Abstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. The Memory Gene,Biomolecules · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Thermal Adaptations in Animals: Genes, Development, and Evolution.Advances in experimental medicine and biology · 2024
    Review
  9. Article
  10. Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Notch Signalling in Breast Development and Cancer.Frontiers in cell and developmental biology · 2021
    Review
  18. Article
  19. Arf6 determines tissue architecture by stabilizing intercellular adhesion.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Hideyuki ShimizuUniversity of Manchester, Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK.
Simon A WoodcockUniversity of Manchester, Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK.
Marian B WilkinUniversity of Manchester, Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK.
Barbora TrubenováUniversity of Manchester, Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK.
Nicholas A M MonkSchool of Mathematics and Statistics, University of Sheffield, Hicks Building, Hounsfield Road, Sheffield S3 7RH, UK.
Martin BaronUniversity of Manchester, Faculty of Life Sciences, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK. Electronic address: mbaron@manchester.ac.uk.

Funding

Biotechnology and Biological Sciences Research Council BB/C503162/1Biotechnology and Biological Sciences Research Council BB/E002285/1Biotechnology and Biological Sciences Research Council BB/H000976/1Biotechnology and Biological Sciences Research Council H000976Wellcome TrustWellcome Trust 087928
6 · The paper itself

Abstract

Developmental signaling is remarkably robust to environmental variation, including temperature. For example, in ectothermic animals such as Drosophila, Notch signaling is maintained within functional limits across a wide temperature range. We combine experimental and computational approaches to show that temperature compensation of Notch signaling is achieved by an unexpected variety of endocytic-dependent routes to Notch activation which, when superimposed on ligand-induced activation, act as a robustness module. Thermal compensation arises through an altered balance of fluxes within competing trafficking routes, coupled with temperature-dependent ubiquitination of Notch. This flexible ensemble of trafficking routes supports Notch signaling at low temperature but can be switched to restrain Notch signaling at high temperature and thus compensates for the inherent temperature sensitivity of ligand-induced activation. The outcome is to extend the physiological range over which normal development can occur. Similar mechanisms may provide thermal robustness for other developmental signals.

Indexed as

EndocytosisAnimalsDown-RegulationDrosophila melanogasterDrosophila ProteinsMembrane ProteinsReceptors, NotchSignal TransductionTemperatureUbiquitin-Protein LigasesDrosophila ProteinsDX protein, DrosophilaMembrane ProteinsN protein, DrosophilaReceptors, NotchSu(dx) protein, DrosophilaUbiquitin-Protein Ligases

Identifiers

PMID24855951
PMCPMC4032575

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.