Evidence map›Paper›PMID 24875805›Full record

ArticlePloS one2014

Notchless is required for axial skeleton formation in mice.

Sarah Beck-Cormier, Marie Escande, Céline Souilhol, Sandrine Vandormael-Pournin, Sophie Sourice, Paul Pilet, Charles Babinet, Michel Cohen-Tannoudji

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

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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 at 2 institutions in 1 country.

Sarah Beck-CormierMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique, URA 2578, Institut Pasteur, Paris, France.
Marie EscandeMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France.
Céline SouilholMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France.
Sandrine Vandormael-PourninMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique, URA 2578, Institut Pasteur, Paris, France.
Sophie SouriceInstitut National de la Santé et de la recherche Médicale, U791, LIOAD, STEP group "Skeletal Tissue Engineering and Physiopathology", Nantes, France.
Paul PiletInstitut National de la Santé et de la recherche Médicale, U791, LIOAD, STEP group "Skeletal Tissue Engineering and Physiopathology", Nantes, France.
Charles BabinetMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique, URA 2578, Institut Pasteur, Paris, France.
Michel Cohen-TannoudjiMouse Functional Genetics, Department of Developmental & Stem Cell Biology, Institut Pasteur, Paris, France; Centre National de la Recherche Scientifique, URA 2578, Institut Pasteur, Paris, France.
Institut Pasteur · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of cell survival is essential for proper embryonic development. In the mouse, Notchless homolog 1 (Drosophila) (Nle1) is instrumental for survival of cells of the inner cell mass upon implantation. Here, we analyze the function of Nle1 after implantation using the Meox2(tm1(cre)Sor) mouse that expresses the Cre recombinase specifically in the epiblast at E5.5. First, we find that NLE1 function is required in epiblast cells, as Nle1-deficient cells are rapidly eliminated. In this report, we also show that the Meox2(Cre) transgene is active in specific tissues during organogenesis. In particular, we detect high Cre expression in the vertebral column, ribs, limbs and tailbud. We took advantage of this dynamic expression profile to analyze the effects of inducing mosaic deletion of Nle1 in the embryo. We show that Nle1 deletion in this context, results in severe developmental anomalies leading to lethality at birth. Mutant embryos display multiple developmental defects in particular during axial skeletal formation. We also provide evidence that axial defects are due to an increase in apoptotic cell death in the somite at E9.5. These data demonstrate an essential role for Nle1 during organogenesis and in particular during axial development.

Indexed as

AnimalsApoptosisCaspase 3Embryo ImplantationEmbryo, MammalianFemaleGene Expression Regulation, DevelopmentalGerm LayersHomeodomain ProteinsMembrane ProteinsMiceMice, TransgenicMicrofilament ProteinsMutationNeural TubeOrganogenesisCaspase 3Homeodomain ProteinsMembrane ProteinsMeox2 protein, mouseMicrofilament Proteinsnotchless protein, mouse

Identifiers

PMID24875805
PMCPMC4038589
OpenAlexW2004672522

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.