Evidence map›Paper›PMID 37162187›Full record

ArticleeLife2023

A ratchet-like apical constriction drives cell ingression during the mouse gastrulation EMT.

Alexandre Francou, Kathryn V Anderson, Anna-Katerina Hadjantonakis

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Opposing Activity at the Apical Surface: An Antagonistic Collaboration Between Crumbs and Myosin II Determines Organ Shape.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  4. Article
  5. Positional information and information flows in dynamic tissues.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Tumors and their microenvironments: Learning from pediatric brain pathologies.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  8. Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025
    Review
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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

3 authors at 1 institution in 1 country.

Alexandre FrancouDevelopmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, United States.ORCID 0000-0002-6295-3777
Kathryn V AndersonDevelopmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, United States.
Anna-Katerina HadjantonakisDevelopmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, United States.ORCID 0000-0002-7580-5124
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
ISOLATION OF NOVEL MUTATIONS AFFECTING THE MOUSE EMBRYOR01HD035455 · NICHD · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI HADJANTONAKIS, ANNA-KATERINA, HUANGFU, DANWEI · 1998 to 2022
$7.1M
Mechanisms driving cell fate specification and morphogenesis in the blastocystR01HD094868 · NICHD · SLOAN-KETTERING INST CAN RESEARCH · PI ANNA-KATERINA HADJANTONAKIS · 2018 to 2026
$4.2M
Phenotyping Early Embryonic Lethal Knockout Mice to Identify Essential Genes with Previously Uncharacterized Roles in Pre-implantation Development, Gastrulation, Turning, and PlacentationR01HD086478 · NICHD · SLOAN-KETTERING INST CAN RESEARCH · PI HADJANTONAKIS, ANNA-KATERINA · 2016 to 2020
$3.4M
The gut endoderm: origin, formation and fateR01DK127821 · NIDDK · SLOAN-KETTERING INST CAN RESEARCH · PI ANNA-KATERINA HADJANTONAKIS · 2021 to 2026
$3.4M
NCI NIH HHS P30 CA008748NICHD NIH HHS R01 HD035455NICHD NIH HHS R01 HD086478NICHD NIH HHS R01 HD094868NIDDK NIH HHS R01 DK127821
6 · The paper itself

Abstract

Epithelial-to-mesenchymal transition (EMT) is a fundamental process whereby epithelial cells acquire mesenchymal phenotypes and the ability to migrate. EMT is the hallmark of gastrulation, an evolutionarily conserved developmental process. In mammals, epiblast cells ingress at the primitive streak to form mesoderm. Cells ingress and exit the epiblast epithelial layer and the associated EMT is dynamically regulated and involves a stereotypical sequence of cell behaviors. 3D time-lapse imaging of gastrulating mouse embryos combined with cell and tissue scale data analyses revealed the asynchronous ingression of epiblast cells at the primitive streak. Ingressing cells constrict their apical surfaces in a pulsed ratchet-like fashion through asynchronous shrinkage of apical junctions. A quantitative analysis of the distribution of apical proteins revealed the anisotropic and reciprocal enrichment of members of the actomyosin network and Crumbs2 complexes, potential regulators of asynchronous shrinkage of cell junctions. Loss of function analyses demonstrated a requirement for Crumbs2 in myosin II localization and activity at apical junctions, and as a candidate regulator of actomyosin anisotropy.

Indexed as

ActomyosinGastrulationAnimalsConstrictionGerm LayersMammalsMesodermMiceActomyosinapical constrictioncell biologycell dynamicsdevelopmental biologyEMTgastrulationmouse

Identifiers

PMID37162187
PMCPMC10171865
OpenAlexW4376131617

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.