Evidence map›Paper›PMID 27065194›Full record

ArticleNature structural & molecular biology2016

BTG4 is a meiotic cell cycle-coupled maternal-zygotic-transition licensing factor in oocytes.

Chao Yu, Shu-Yan Ji, Qian-Qian Sha, Yujiao Dang, Jian-Jie Zhou, Yin-Li Zhang, Yang Liu, Zhong-Wei Wang, Boqiang Hu, Qing-Yuan Sun and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 2% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 273 citations in OpenAlex.

  1. Pooled it
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  6. Single-molecule mbioRxiv : the preprint server for biology · 2026
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96 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Chao YuLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Shu-Yan JiLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Qian-Qian ShaLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Yujiao DangBiodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing, China.
Jian-Jie ZhouLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Yin-Li ZhangLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Yang LiuLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Zhong-Wei WangState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Boqiang HuBiodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing, China.
Qing-Yuan SunState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Shao-Chen SunCollege of Animal Science and Technology, Nanjing Agricultural University, Nanjing, China.
Fuchou TangBiodynamic Optical Imaging Center, College of Life Sciences, Peking University, Beijing, China.
Heng-Yu FanLife Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
Zhejiang University · CNPeking University · CNChinese Academy of Sciences · CNNanjing Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mRNAs stored in oocytes undergo general decay during the maternal-zygotic transition (MZT), and their stability is tightly interconnected with meiotic cell-cycle progression. However, the factors that trigger decay of maternal mRNA and couple this event to oocyte meiotic maturation remain elusive. Here, we identified B-cell translocation gene-4 (BTG4) as an MZT licensing factor in mice. BTG4 bridged CNOT7, a catalytic subunit of the CCR4-NOT deadenylase, to eIF4E, a key translation initiation factor, and facilitated decay of maternal mRNA. Btg4-null females produced morphologically normal oocytes but were infertile, owing to early developmental arrest. The intrinsic MAP kinase cascade in oocytes triggered translation of Btg4 mRNA stored in fully grown oocytes by targeting the 3' untranslated region, thereby coupling CCR4-NOT deadenylase-mediated decay of maternal mRNA with oocyte maturation and fertilization. This is a key step in oocyte cytoplasmic maturation that determines the developmental potential of mammalian embryos.

Indexed as

3' Untranslated RegionsAnimalsBase SequenceCell Cycle ProteinsCells, CulturedEukaryotic Initiation Factor-4EExoribonucleasesFemaleGene ExpressionGene Expression Regulation, DevelopmentalGene Knockout TechniquesMaleMAP Kinase Signaling SystemMeiosisMice, Inbred ICRMice, Knockout3' Untranslated RegionsBtg4 protein, mouseCell Cycle ProteinsCnot7 protein, mouseeIF4E protein, mouseEukaryotic Initiation Factor-4EExoribonucleasesProteinsRepressor ProteinsRibonucleases

Identifiers

PMID27065194
OpenAlexW2326766364

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.