Evidence map›Paper›PMID 36509125›Full record

ArticleDevelopmental biology2023

Synchronisation of apical constriction and cell cycle progression is a conserved behaviour of pseudostratified neuroepithelia informed by their tissue geometry.

Ioakeim Ampartzidis, Christoforos Efstathiou, Francesco Paonessa, Elliott M Thompson, Tyler Wilson, Conor J McCann, Nicholas DE Greene, Andrew J Copp, Frederick J Livesey, Nicola Elvassore and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

14 authors at 4 institutions in 4 countries.

Ioakeim AmpartzidisDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Christoforos EfstathiouDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Francesco PaonessaDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; UCL Great Ormond Street Institute of Child Health, Zayed Centre for Research Into Rare Disease in Children, London, UK.
Elliott M ThompsonDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Tyler WilsonDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Conor J McCannDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Nicholas DE GreeneDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Andrew J CoppDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Frederick J LiveseyDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; UCL Great Ormond Street Institute of Child Health, Zayed Centre for Research Into Rare Disease in Children, London, UK.
Nicola ElvassoreDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; Veneto Institute of Molecular Medicine, Padova, Italy; UCL Great Ormond Street Institute of Child Health, Zayed Centre for Research Into Rare Disease in Children, London, UK.
Giovanni G GiobbeDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; UCL Great Ormond Street Institute of Child Health, Zayed Centre for Research Into Rare Disease in Children, London, UK.
Paolo De CoppiDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; UCL Great Ormond Street Institute of Child Health, Zayed Centre for Research Into Rare Disease in Children, London, UK; Specialist Neonatal and Paediatric Unit, Great Ormond Street Hospital, London, WC1N 1EH, UK.
Eirini ManiouDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK; Veneto Institute of Molecular Medicine, Padova, Italy.
Gabriel L GaleaDevelopmental Biology and Cancer Department, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK. Electronic address: g.galea@ucl.ac.uk.
University College London · GBGreat Ormond Street Hospital · GBInstitute of Child Health · GRVeneto Institute of Molecular Medicine · IT

Funding

Medical Research Council MC_EX_MR/N50192X/1Wellcome Trust
6 · The paper itself

Abstract

Neuroepithelial cells balance tissue growth requirement with the morphogenetic imperative of closing the neural tube. They apically constrict to generate mechanical forces which elevate the neural folds, but are thought to apically dilate during mitosis. However, we previously reported that mitotic neuroepithelial cells in the mouse posterior neuropore have smaller apical surfaces than non-mitotic cells. Here, we document progressive apical enrichment of non-muscle myosin-II in mitotic, but not non-mitotic, neuroepithelial cells with smaller apical areas. Live-imaging of the chick posterior neuropore confirms apical constriction synchronised with mitosis, reaching maximal constriction by anaphase, before division and re-dilation. Mitotic apical constriction amplitude is significantly greater than interphase constrictions. To investigate conservation in humans, we characterised early stages of iPSC differentiation through dual SMAD-inhibition to robustly produce pseudostratified neuroepithelia with apically enriched actomyosin. These cultured neuroepithelial cells achieve an equivalent apical area to those in mouse embryos. iPSC-derived neuroepithelial cells have large apical areas in G2 which constrict in M phase and retain this constriction in G1/S. Given that this differentiation method produces anterior neural identities, we studied the anterior neuroepithelium of the elevating mouse mid-brain neural tube. Instead of constricting, mid-brain mitotic neuroepithelial cells have larger apical areas than interphase cells. Tissue geometry differs between the apically convex early midbrain and flat posterior neuropore. Culturing human neuroepithelia on equivalently convex surfaces prevents mitotic apical constriction. Thus, neuroepithelial cells undergo high-amplitude apical constriction synchronised with cell cycle progression but the timing of their constriction if influenced by tissue geometry.

Indexed as

MitosisNervous SystemAnimalsCell CycleCell DifferentiationConstrictionHumansMiceApical constrictionChickInterkinetic nuclear migrationiPSCMouseNeuroepithelium

Identifiers

PMID36509125
PMCPMC10570144
OpenAlexW4311754170

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.