Evidence map›Paper›PMID 29731302›Full record

ArticleCurrent biology : CB2018

Quantitative Control of GPCR Organization and Signaling by Endocytosis in Epithelial Morphogenesis.

Ankita Jha, Thomas S van Zanten, Jean-Marc Philippe, Satyajit Mayor, Thomas Lecuit

Open access · greenAbstract read
In one paragraph

Article in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Molecular biology of the cell · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Interplay between mechanics and signalling in regulating cell fate.Nature reviews. Molecular cell biology · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Orthogonal Peptide-Templated Labeling Elucidates Lateral ETChembiochem : a European journal of chemical biology · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. TheMolecular biology of the cell · 2020
    Article
  18. Review
  19. Review
  20. Review
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 2 institutions in 2 countries.

Ankita JhaAix Marseille Université, CNRS, IBDM - UMR7288, Turing Centre for Living Systems, Marseille, France.
Thomas S van ZantenNational Centre for Biological Sciences, TIFR, Bangalore 560065, India.
Jean-Marc PhilippeAix Marseille Université, CNRS, IBDM - UMR7288, Turing Centre for Living Systems, Marseille, France.
Satyajit MayorNational Centre for Biological Sciences, TIFR, Bangalore 560065, India.
Thomas LecuitAix Marseille Université, CNRS, IBDM - UMR7288, Turing Centre for Living Systems, Marseille, France; Collège de France, 11 Place Marcelin Berthelot, Paris, France. Electronic address: thomas.lecuit@univ-amu.fr.
Centre National de la Recherche Scientifique · FRNational Centre for Biological Sciences · IN

Funding

DBT-Wellcome Trust India Alliance IA/M/15/1/502018Wellcome Trust
6 · The paper itself

Abstract

Tissue morphogenesis arises from controlled cell deformations in response to cellular contractility. During Drosophila gastrulation, apical activation of the actomyosin networks drives apical constriction in the invaginating mesoderm and cell-cell intercalation in the extending ectoderm. Myosin II (MyoII) is activated by cell-surface G protein-coupled receptors (GPCRs), such as Smog and Mist, that activate G proteins, the small GTPase Rho1, and the kinase Rok. Quantitative control over GPCR and Rho1 activation underlies differences in deformation of mesoderm and ectoderm cells. We show that GPCR Smog activity is concentrated on two different apical plasma membrane compartments, i.e., the surface and plasma membrane invaginations. Using fluorescence correlation spectroscopy, we probe the surface of the plasma membrane, and we show that Smog homo-clusters in response to its activating ligand Fog. Endocytosis of Smog is regulated by the kinase Gprk2 and β-arrestin-2 that clears active Smog from the plasma membrane. When Fog concentration is high or endocytosis is low, Smog rearranges in homo-clusters and accumulates in plasma membrane invaginations that are hubs for Rho1 activation. Lastly, we find higher Smog homo-cluster concentration and numerous apical plasma membrane invaginations in the mesoderm compared to the ectoderm, indicative of reduced endocytosis. We identify that dynamic partitioning of active Smog at the surface of the plasma membrane or plasma membrane invaginations has a direct impact on Rho1 signaling. Plasma membrane invaginations accumulate high Rho1-guanosine triphosphate (GTP) suggesting they form signaling centers. Thus, Fog concentration and Smog endocytosis form coupled regulatory processes that regulate differential Rho1 and MyoII activation in the Drosophila embryo.

Indexed as

EndocytosisMorphogenesisAnimalsDrosophila melanogasterEpitheliumSignal Transductionacto-myosin contractilityendocytosisepithelial morphogenesisfluorescence correlation spectroscopygastrulationG protein-coupled receptorG protein-coupled receptor kinaseβ-arrestin

Identifiers

PMID29731302
PMCPMC6934411
OpenAlexW2801478675

What OpenQuestion holds

Textmetadata
LicenceTDM
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.