Evidence map›Paper›PMID 23221368›Full record

ArticleDevelopment (Cambridge, England)2013

Nodal/activin signaling promotes male germ cell fate and suppresses female programming in somatic cells.

Quan Wu, Kohei Kanata, Rie Saba, Chu-Xia Deng, Hiroshi Hamada, Yumiko Saga

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 64 citations in OpenAlex.

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  13. The TGF-β Family in the Reproductive Tract.Cold Spring Harbor perspectives in biology · 2017
    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

6 authors at 4 institutions in 2 countries.

Quan WuDepartment of Genetics, SOKENDAI, Yata 1111, Mishima 411-8540, Japan.
Kohei Kanata
Rie Saba
Chu-Xia Deng
Hiroshi Hamada
Yumiko Saga
National Institute of Genetics · JPOsaka University · JPNational Institute of Diabetes and Digestive and Kidney Diseases · USThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Testicular development in the mouse is triggered in somatic cells by the function of Sry followed by the activation of fibroblast growth factor 9 (FGF9), which regulates testicular differentiation in both somatic and germ cells. However, the mechanism is unknown. We show here that the nodal/activin signaling pathway is activated in both male germ cells and somatic cells. Disruption of nodal/activin signaling drives male germ cells into meiosis and causes ectopic initiation of female-specific genes in somatic cells. Furthermore, we prove that nodal/activin-A works directly on male germ cells to induce the male-specific gene Nanos2 independently of FGF9. We conclude that nodal/activin signaling is required for testicular development and propose a model in which nodal/activin-A acts downstream of fibroblast growth factor signaling to promote male germ cell fate and protect somatic cells from initiating female differentiation.

Indexed as

Cell DifferentiationGene Expression Regulation, DevelopmentalActivinsAnimalsCarrier ProteinsFemaleFibroblast Growth Factor 9Germ CellsLeft-Right Determination FactorsMaleMiceMice, Inbred ICRMice, KnockoutNodal ProteinOligonucleotide Array Sequence AnalysisRNA-Binding ProteinsActivinsCarrier ProteinsFibroblast Growth Factor 9Left-Right Determination FactorsLefty1 protein, mouseLefty2 protein, mouseNanos2 protein, mouseNodal ProteinRNA-Binding Proteins

Identifiers

PMID23221368
PMCPMC3597207
OpenAlexW1979106724

What OpenQuestion holds

Textmetadata
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.