Evidence map›Paper›PMID 36197846›Full record

ArticlePLoS genetics2022

The RNA helicase DDX6 controls early mouse embryogenesis by repressing aberrant inhibition of BMP signaling through miRNA-mediated gene silencing.

Jessica Kim, Masafumi Muraoka, Hajime Okada, Atsushi Toyoda, Rieko Ajima, Yumiko Saga

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 16 citations in OpenAlex.

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  6. Role of TLRs as signaling cascades to combat infectious diseases: a review.Cellular and molecular life sciences : CMLS · 2025
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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 2 institutions in 1 country.

Jessica KimDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9795-2275
Masafumi MuraokaMammalian Development Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, Mishima, Japan.ORCID 0000-0003-2409-9837
Hajime OkadaMammalian Development Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, Mishima, Japan.ORCID 0000-0002-3204-3633
Atsushi ToyodaAdvanced Genomics Center, National Institute of Genetics, Mishima, Japan.ORCID 0000-0002-0728-7548
Rieko AjimaMammalian Development Laboratory, Department of Gene Function and Phenomics, National Institute of Genetics, Mishima, Japan.ORCID 0000-0001-9740-2660
Yumiko SagaDepartment of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9198-5164
National Institute of Genetics · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evolutionarily conserved RNA helicase DDX6 is a central player in post-transcriptional regulation, but its role during embryogenesis remains elusive. We here show that DDX6 enables proper cell lineage specification from pluripotent cells by analyzing Ddx6 knockout (KO) mouse embryos and employing an in vitro epiblast-like cell (EpiLC) induction system. Our study unveils that DDX6 is an important BMP signaling regulator. Deletion of Ddx6 causes the aberrant upregulation of the negative regulators of BMP signaling, which is accompanied by enhanced expression of Nodal and related genes. Ddx6 KO pluripotent cells acquire higher pluripotency with a strong inclination toward neural lineage commitment. During gastrulation, abnormally expanded Nodal and Eomes expression in the primitive streak likely promotes endoderm cell fate specification while inhibiting mesoderm differentiation. We also genetically dissected major DDX6 pathways by generating Dgcr8, Dcp2, and Eif4enif1 KO models in addition to Ddx6 KO. We found that the miRNA pathway mutant Dgcr8 KO phenocopies Ddx6 KO, indicating that DDX6 mostly works along with the miRNA pathway during early development, whereas its P-body-related functions are dispensable. Therefore, we conclude that DDX6 prevents aberrant upregulation of BMP signaling inhibitors by participating in miRNA-mediated gene silencing processes. Overall, this study delineates how DDX6 affects the development of the three primary germ layers during early mouse embryogenesis and the underlying mechanism of DDX6 function.

Indexed as

GastrulationMicroRNAsAnimalsBone Morphogenetic ProteinsCell DifferentiationDEAD-box RNA HelicasesGene SilencingMiceProto-Oncogene ProteinsRNA-Binding ProteinsTransforming Growth Factor betaBone Morphogenetic ProteinsDdx6 protein, mouseDEAD-box RNA HelicasesMicroRNAsProto-Oncogene ProteinsRNA-Binding ProteinsTransforming Growth Factor beta

Identifiers

PMID36197846
PMCPMC9534413
OpenAlexW4302012134

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.