Evidence map›Paper›PMID 27065197›Full record

ArticleNature structural & molecular biology2016

Mammalian elongation factor 4 regulates mitochondrial translation essential for spermatogenesis.

Yanyan Gao, Xiufeng Bai, Dejiu Zhang, Chunsheng Han, Jing Yuan, Wenbin Liu, Xintao Cao, Zilei Chen, Fugen Shangguan, Zhenyuan Zhu and 2 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 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  14. BAF-L Modulates Histone-to-Protamine Transition during Spermiogenesis.International journal of molecular sciences · 2022
    Article
  15. Mitochondrial regulation during male germ cell development.Cellular and molecular life sciences : CMLS · 2022
    Review
  16. Article
  17. Functions and Regulation of Translation Elongation Factors.Frontiers in molecular biosciences · 2021
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 1 country.

Yanyan GaoKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Xiufeng BaiKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Dejiu ZhangKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Chunsheng HanUniversity of Chinese Academy of Sciences, Beijing, China.
Jing YuanInstitute of Disease Control and Prevention, Academy of Military Medical Sciences, Beijing, China.
Wenbin LiuKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Xintao CaoKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Zilei ChenKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Fugen ShangguanKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Zhenyuan ZhuKey Laboratory of Food Nutrition and Safety, Ministry of Education, School of Food Engineering and Biotechnology, Tianjin University of Science and Technology, Tianjin, China.
Fei GaoUniversity of Chinese Academy of Sciences, Beijing, China.
Yan QinKey Laboratory of RNA Biology, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Institute of Biophysics · CNChinese Academy of Sciences · CNAcademy of Military Medical Sciences · CNTianjin University of Science and Technology · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elongation factor 4 (EF4) is a key quality-control factor in translation. Despite its high conservation throughout evolution, EF4 deletion in various organisms has not yielded a distinct phenotype. Here we report that genetic ablation of mitochondrial EF4 (mtEF4) in mice causes testis-specific dysfunction in oxidative phosphorylation, leading to male infertility. Deletion of mtEF4 accelerated mitochondrial translation at the cost of producing unstable proteins. Somatic tissues overcame this defect by activating mechanistic (mammalian) target of rapamycin (mTOR), thereby increasing rates of cytoplasmic translation to match rates of mitochondrial translation. However, in spermatogenic cells, the mTOR pathway was downregulated as part of the developmental program, and the resulting inability to compensate for accelerated mitochondrial translation caused cell-cycle arrest and apoptosis. We detected the same phenotype and molecular defects in germline-specific mtEF4-knockout mice. Thus, our study demonstrates cross-talk between mtEF4-dependent quality control in mitochondria and cytoplasmic mTOR signaling.

Indexed as

Protein BiosynthesisSpermatogenesis3T3 CellsAnimalsFemaleGene Expression RegulationInfertility, MaleMaleMiceMice, KnockoutMitochondriaOxidative PhosphorylationPeptide Initiation FactorsProtein TransportRibosomesTestisPeptide Initiation Factors

Identifiers

PMID27065197
OpenAlexW2319020867

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.