Evidence map›Paper›PMID 39382697›Full record

ArticleCellular and molecular life sciences : CMLS2024

Silencing of maternally expressed RNAs in Dlk1-Dio3 domain causes fatal vascular injury in the fetal liver.

Haoran Yu, Yue Zhao, Rui Cheng, Mengyun Wang, Xin Hu, Ximeijia Zhang, Xiangqi Teng, Hongjuan He, Zhengbin Han, Xiao Han and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Haoran YuSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Yue ZhaoDepartment of Urology, School of Medicine, Xiang'an Hospital of Xiamen University, Xiamen University, Xiamen, 361000, China.
Rui ChengState Key Laboratory for Conservation and Utilization of Bio-Resource and School of Life Sciences, Yunnan University, Kunming, 650091, China.
Mengyun WangSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Xin HuSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Ximeijia ZhangSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Xiangqi TengSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Hongjuan HeSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Zhengbin HanHIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China.
Xiao HanSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Ziwen WangSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Bingjing LiuSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China.
Yan ZhangComputational Biology Research Center, School of Life Science and Technology, Harbin Institute of Technology, Harbin, 150001, China. zhangtyo@hit.edu.cn.
Qiong WuSchool of Life Science and Technology, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin, 150001, China. kigo@hit.edu.cn.ORCID http://orcid.org/0000-0003-3305-6652

Funding

Innovative Research Group Project of the National Natural Science Foundation of China U20A20376Key Research and Development Program of Heilongjiang 2023ZX06C09State Key Laboratory of Urban Water Resource and Environment 2022TS27
6 · The paper itself

Abstract

The mammalian imprinted Dlk1-Dio3 domain contains multiple lncRNAs, mRNAs, the largest miRNA cluster in the genome and four differentially methylated regions (DMRs), and deletion of maternally expressed RNA within this locus results in embryonic lethality, but the mechanism by which this occurs is not clear. Here, we optimized the model of maternally expressed RNAs transcription termination in the domain and found that the cause of embryonic death was apoptosis in the embryo, particularly in the liver. We generated a mouse model of maternally expressed RNAs silencing in the Dlk1-Dio3 domain by inserting a 3 × polyA termination sequence into the Gtl2 locus. By analyzing RNA-seq data of mouse embryos combined with histological analysis, we found that silencing of maternally expressed RNAs in the domain activated apoptosis, causing vascular rupture of the fetal liver, resulting in hemorrhage and injury. Mechanistically, termination of Gtl2 transcription results in the silencing of maternally expressed RNAs and activation of paternally expressed genes in the interval, and it is the gene itself rather than the IG-DMR and Gtl2-DMR that causes the aforementioned phenotypes. In conclusion, these findings illuminate a novel mechanism by which the silencing of maternally expressed RNAs within Dlk1-Dio3 domain leads to hepatic hemorrhage and embryonic death through the activation of apoptosis.

Indexed as

ApoptosisCalcium-Binding ProteinsIodide PeroxidaseLiverRNA, Long NoncodingAnimalsDNA MethylationEmbryo, MammalianFemaleFetusGene Expression Regulation, DevelopmentalGene SilencingGenomic ImprintingIntercellular Signaling Peptides and ProteinsMaleMiceCalcium-Binding ProteinsDlk1 protein, mouseIntercellular Signaling Peptides and ProteinsIodide Peroxidaseiodothyronine deiodinase type IIIMEG3 non-coding RNA, mouseRNA, Long NoncodingEasi-CRISPREmbryonic lethalityLong non-coding RNAsMaternally expressed RNAsMouse

Identifiers

PMID39382697
PMCPMC11465015

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.