Evidence map›Paper›PMID 28654702›Full record

ArticlePloS one2017

Stomatin-like protein 2 deficiency results in impaired mitochondrial translation.

Panagiotis Mitsopoulos, Orsolya Lapohos, Woranontee Weraarpachai, Hana Antonicka, Yu-Han Chang, Joaquín Madrenas

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

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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

6 authors at 2 institutions in 3 countries.

Panagiotis MitsopoulosMicrobiome and Disease Tolerance Centre, Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Orsolya LapohosMicrobiome and Disease Tolerance Centre, Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Woranontee WeraarpachaiDepartment of Human Genetics and Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Hana AntonickaDepartment of Human Genetics and Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Yu-Han ChangMicrobiome and Disease Tolerance Centre, Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.
Joaquín MadrenasMicrobiome and Disease Tolerance Centre, Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada.ORCID http://orcid.org/0000-0001-6191-3733
The Lundquist Institute · USMontreal Neurological Institute and Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria translate the RNAs for 13 core polypeptides of respiratory chain and ATP synthase complexes that are essential for the assembly and function of these complexes. This process occurs in close proximity to the mitochondrial inner membrane. However, the mechanisms and molecular machinery involved in mitochondrial translation are not fully understood, and defects in this process can result in severe diseases. Stomatin-like protein (SLP)-2 is a mainly mitochondrial protein that forms cardiolipin- and prohibitin-enriched microdomains in the mitochondrial inner membrane that are important for the formation of respiratory supercomplexes and their function. Given this regulatory role of SLP-2 in processes closely associated with the mitochondrial inner membrane, we hypothesized that the function of SLP-2 would have an impact on mitochondrial translation. 35S-Methionine/cysteine pulse labeling of resting or activated T cells from T cell-specific Slp-2 knockout mice showed a significant impairment in the production of several mitochondrial DNA-encoded polypeptides following T cell activation, including Cytb, COXI, COXII, COXIII, and ATP6. Measurement of mitochondrial DNA stability and mitochondrial transcription revealed that this impairment was at the post-transcriptional level. Examination of mitochondrial ribosome assembly showed that SLP-2 migrated in sucrose-density gradients similarly to the large ribosomal subunit but that its deletion at the genetic level did not affect mitochondrial ribosome assembly. Functionally, the impairment in mitochondrial translation correlated with decreased interleukin-2 production in activated T cells. Altogether, these data show that SLP-2 acts as a general regulator of mitochondrial translation.

Indexed as

Protein BiosynthesisAnimalsLymphocyte ActivationMembrane ProteinsMiceMice, KnockoutMitochondriaMitochondrial MembranesMitochondrial ProteinsNerve Tissue ProteinsT-LymphocytesMembrane ProteinsMitochondrial ProteinsNerve Tissue Proteinsstomatin-like protein 2, mouse

Identifiers

PMID28654702
PMCPMC5487072
OpenAlexW2725377668

What OpenQuestion holds

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LicenceCC BY
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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.