Evidence map›Paper›PMID 23572076›Full record

ArticleThe EMBO journal2013

Mitochondria-type GPAT is required for mitochondrial fusion.

Yohsuke Ohba, Takeshi Sakuragi, Eriko Kage-Nakadai, Naoko H Tomioka, Nozomu Kono, Rieko Imae, Asuka Inoue, Junken Aoki, Naotada Ishihara, Takao Inoue and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genome-wide analysis of theFrontiers in plant science · 2026
    Article
  5. Molecular mechanisms of mitochondrial dynamics.Nature reviews. Molecular cell biology · 2025
    Review
  6. Article
  7. Article
  8. Genome-Wide Identification of the GPAT Family inPlants (Basel, Switzerland) · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Phospholipid ebb and flow makes mitochondria go.The Journal of cell biology · 2020
    Review
  14. Mitochondrial Morphofunction in Mammalian Cells.Antioxidants & redox signaling · 2019
    Review
  15. Article
  16. Review
  17. Understanding the diversity of membrane lipid composition.Nature reviews. Molecular cell biology · 2018
    Review
  18. Review
  19. Sequences flanking the transmembrane segments facilitate mitochondrial localization and membrane fusion by mitofusin.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  20. Review
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

12 authors at 5 institutions in 1 country.

Yohsuke OhbaDepartment of Health Chemistry, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo, Japan.
Takeshi Sakuragi
Eriko Kage-Nakadai
Naoko H Tomioka
Nozomu Kono
Rieko Imae
Asuka Inoue
Junken Aoki
Naotada Ishihara
Takao Inoue
Shohei Mitani
Hiroyuki Arai
University of Tokyo Health Sciences · JPJapan Science and Technology Agency · JPTohoku University · JPTokyo Women's Medical University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycerol-3-phosphate acyltransferase (GPAT) is involved in the first step in glycerolipid synthesis and is localized in both the endoplasmic reticulum (ER) and mitochondria. To clarify the functional differences between ER-GPAT and mitochondrial (Mt)-GPAT, we generated both GPAT mutants in C. elegans and demonstrated that Mt-GPAT is essential for mitochondrial fusion. Mutation of Mt-GPAT caused excessive mitochondrial fragmentation. The defect was rescued by injection of lysophosphatidic acid (LPA), a direct product of GPAT, and by inhibition of LPA acyltransferase, both of which lead to accumulation of LPA in the cells. Mitochondrial fragmentation in Mt-GPAT mutants was also rescued by inhibition of mitochondrial fission protein DRP-1 and by overexpression of mitochondrial fusion protein FZO-1/mitofusin, suggesting that the fusion/fission balance is affected by Mt-GPAT depletion. Mitochondrial fragmentation was also observed in Mt-GPAT-depleted HeLa cells. A mitochondrial fusion assay using HeLa cells revealed that Mt-GPAT depletion impaired mitochondrial fusion process. We postulate from these results that LPA produced by Mt-GPAT functions not only as a precursor for glycerolipid synthesis but also as an essential factor of mitochondrial fusion.

Indexed as

Mitochondrial DynamicsAnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsFemaleGene DeletionGlycerol-3-Phosphate O-AcyltransferaseLysophospholipidsMicrosomesMitochondriaMitochondrial SizeModels, BiologicalMutagenesis, Site-DirectedOogenesisAcl-6 protein, C elegansCaenorhabditis elegans ProteinsGlycerol-3-Phosphate O-Acyltransferaselysophosphatidic acidLysophospholipids

Identifiers

PMID23572076
PMCPMC3642685
OpenAlexW1999332554

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.