Evidence map›Paper›PMID 33028844›Full record

ArticleNature communications2020

Tracing the cellular basis of islet specification in mouse pancreas.

Magdalena K Sznurkowska, Edouard Hannezo, Roberta Azzarelli, Lemonia Chatzeli, Tatsuro Ikeda, Shosei Yoshida, Anna Philpott, Benjamin D Simons

Abstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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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

8 authors.

Magdalena K Sznurkowska *Department of Oncology, University of Cambridge, Hutchison/MRC Research Centre, Cambridge Biomedical Campus, Cambridge, CB2 0XZ, UK.
Edouard Hannezo *IST Austria, Am Campus 1, 3400, Klosterneuburg, Austria.ORCID http://orcid.org/0000-0001-6005-1561
Roberta AzzarelliDepartment of Oncology, University of Cambridge, Hutchison/MRC Research Centre, Cambridge Biomedical Campus, Cambridge, CB2 0XZ, UK.ORCID http://orcid.org/0000-0002-8160-7538
Lemonia ChatzeliWellcome Trust/Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QR, UK.
Tatsuro IkedaDivision of Germ Cell Biology, National Institute for Basic Biology, National Institutes of Natural Sciences, 5-1 Higashiyama, Myodaiji, Okazaki, 444-8787, Japan.ORCID http://orcid.org/0000-0002-8503-8096
Shosei YoshidaDivision of Germ Cell Biology, National Institute for Basic Biology, National Institutes of Natural Sciences, 5-1 Higashiyama, Myodaiji, Okazaki, 444-8787, Japan.ORCID http://orcid.org/0000-0001-8861-1866
Anna PhilpottDepartment of Oncology, University of Cambridge, Hutchison/MRC Research Centre, Cambridge Biomedical Campus, Cambridge, CB2 0XZ, UK. ap113@cam.ac.uk.ORCID http://orcid.org/0000-0003-3789-2463
Benjamin D SimonsWellcome Trust/Medical Research Council Cambridge Stem Cell Institute, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QR, UK. bds10@cam.ac.uk.ORCID http://orcid.org/0000-0002-3875-7071

Funding

Medical Research Council MC_PC_12009Medical Research Council MC_PC_17230Medical Research Council MR/K018329/1Wellcome TrustWellcome Trust 092096/Z/11/ZWellcome Trust 097922/Z/11/ZWellcome Trust 098357/Z/12/ZWellcome Trust 110326/Z/15/Z
6 · The paper itself

Abstract

Pancreatic islets play an essential role in regulating blood glucose level. Although the molecular pathways underlying islet cell differentiation are beginning to be resolved, the cellular basis of islet morphogenesis and fate allocation remain unclear. By combining unbiased and targeted lineage tracing, we address the events leading to islet formation in the mouse. From the statistical analysis of clones induced at multiple embryonic timepoints, here we show that, during the secondary transition, islet formation involves the aggregation of multiple equipotent endocrine progenitors that transition from a phase of stochastic amplification by cell division into a phase of sublineage restriction and limited islet fission. Together, these results explain quantitatively the heterogeneous size distribution and degree of polyclonality of maturing islets, as well as dispersion of progenitors within and between islets. Further, our results show that, during the secondary transition, α- and β-cells are generated in a contemporary manner. Together, these findings provide insight into the cellular basis of islet development.

Indexed as

Cell DifferentiationAnimalsCell LineageComputer SimulationEmbryo, MammalianEmbryonic DevelopmentFemaleGenes, ReporterGlucagon-Secreting CellsImaging, Three-DimensionalInsulin-Secreting CellsLuminescent ProteinsMaleMiceMice, TransgenicMicroscopy, ConfocalLuminescent Proteins

Identifiers

PMID33028844
PMCPMC7541446

What OpenQuestion holds

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LicenceCC BY
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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.