Evidence map›Paper›PMID 22433850›Full record

ArticleThe Journal of biological chemistry2012

Cardiolipin and mitochondrial phosphatidylethanolamine have overlapping functions in mitochondrial fusion in Saccharomyces cerevisiae.

Amit S Joshi, Morgan N Thompson, Naomi Fei, Maik Hüttemann, Miriam L Greenberg

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed
8.3field-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

119 citing papers in PubMed, 197 citations in OpenAlex.

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  17. The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Review
  18. Article
  19. Review
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59 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Amit S JoshiDepartment of Biological Sciences, Wayne State University, Detroit, Michigan 48202 and.
Morgan N ThompsonDepartment of Biological Sciences, Wayne State University, Detroit, Michigan 48202 and.
Naomi FeiDepartment of Biological Sciences, Wayne State University, Detroit, Michigan 48202 and.
Maik HüttemannCenter for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan 48201.
Miriam L GreenbergDepartment of Biological Sciences, Wayne State University, Detroit, Michigan 48202 and. Electronic address: mlgreen@sun.science.wayne.edu.
Wayne State University · US

Funding

SYNTHETIC LETHAL INTERACTIONS IN BARTH SYNDROMER21HL084218 · NHLBI · WAYNE STATE UNIVERSITY · PI GREENBERG, MIRIAM L · 2008 to 2009
$414k
NHLBI NIH HHS R21 HL 084218NHLBI NIH HHS R21 HL084218
6 · The paper itself

Abstract

The two non-bilayer forming mitochondrial phospholipids cardiolipin (CL) and phosphatidylethanolamine (PE) play crucial roles in maintaining mitochondrial morphology. We have shown previously that CL and PE have overlapping functions, and the loss of both is synthetically lethal. Because the lack of CL does not lead to defects in the mitochondrial network in Saccharomyces cerevisiae, we hypothesized that PE may compensate for CL in the maintenance of mitochondrial tubular morphology and fusion. To test this hypothesis, we constructed a conditional mutant crd1Δpsd1Δ containing null alleles of CRD1 (CL synthase) and PSD1 (mitochondrial phosphatidylserine decarboxylase), in which the wild type CRD1 gene is expressed on a plasmid under control of the TET(OFF) promoter. In the presence of tetracycline, the mutant exhibited highly fragmented mitochondria, loss of mitochondrial DNA, and reduced membrane potential, characteristic of fusion mutants. Deletion of DNM1, required for mitochondrial fission, restored the tubular mitochondrial morphology. Loss of CL and mitochondrial PE led to reduced levels of small and large isoforms of the fusion protein Mgm1p, possibly accounting for the fusion defect. Taken together, these data demonstrate for the first time in vivo that CL and mitochondrial PE are required to maintain tubular mitochondrial morphology and have overlapping functions in mitochondrial fusion.

Indexed as

Carboxy-LyasesCardiolipinsGTP-Binding ProteinsMembrane FusionMembrane Potential, MitochondrialMembrane ProteinsMitochondriaMitochondrial MembranesMitochondrial ProteinsPhosphatidylethanolaminesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTransferases (Other Substituted Phosphate Groups)Carboxy-LyasesCardiolipinscardiolipin synthetaseGTP-Binding ProteinsMembrane ProteinsMGM1 protein, S cerevisiaeMitochondrial ProteinsphosphatidylethanolaminePhosphatidylethanolaminesphosphatidylserine decarboxylaseSaccharomyces cerevisiae ProteinsTransferases (Other Substituted Phosphate Groups)

Identifiers

PMID22433850
PMCPMC3366806
OpenAlexW2044769030

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.