Evidence map›Paper›PMID 24610944›Full record

ArticleJournal of cell science2014

Rapamycin increases mitochondrial efficiency by mtDNA-dependent reprogramming of mitochondrial metabolism in Drosophila.

Eugenia Villa-Cuesta, Marissa A Holmbeck, David M Rand

Abstract read
In one paragraph

Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

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  11. Pan-genome survey ofFrontiers in microbiology · 2024
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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

3 authors at 2 institutions in 1 country.

Eugenia Villa-CuestaDepartment of Biology, Adelphi University, PO Box 701, Garden City, NY 11530-0701, USA evilla-cuesta@adelphi.edu.
Marissa A HolmbeckDepartment of Ecology and Evolutionary Biology, Brown University, Box G-W, Providence, RI 02912, USA.
David M RandDepartment of Ecology and Evolutionary Biology, Brown University, Box G-W, Providence, RI 02912, USA.
Brown University · USAdelphi University · US

Funding

Nuclear-Mitochondrial Fitness Interactions in DrosophilaR01GM067862 · NIGMS · BROWN UNIVERSITY · PI RAND, DAVID M · 2004 to 2020
$5.1M
Mitochondrial Genetics of Aging in DrosophilaR01AG027849 · NIA · BROWN UNIVERSITY · PI RAND, DAVID M · 2009 to 2013
$1.5M
A Mitochondrial Hub for Dietary Restriction and AgingF31AG040925 · NIA · BROWN UNIVERSITY · PI HOLMBECK, MARISSA · 2011 to 2013
$79k
NIA NIH HHS 5R01AG027849NIA NIH HHS F31 AG040925NIA NIH HHS R01 AG027849NIGMS NIH HHS R01 GM067862NIGMS NIH HHS R01GM067862
6 · The paper itself

Abstract

Downregulation of the mammalian target of rapamycin (mTOR) pathway by its inhibitor rapamycin is emerging as a potential pharmacological intervention that mimics the beneficial effects of dietary restriction. Modulation of mTOR has diverse effects on mitochondrial metabolism and biogenesis, but the role of the mitochondrial genotype in mediating these effects remains unknown. Here, we use novel mitochondrial genome replacement strains in Drosophila to test the hypothesis that genes encoded in mitochondrial DNA (mtDNA) influence the mTOR pathway. We show that rapamycin increases mitochondrial respiration and succinate dehydrogenase activity, decreases H2O2 production and generates distinct shifts in the metabolite profiles of isolated mitochondria versus whole Drosophila. These effects are disabled when divergent mitochondrial genomes from D. simulans are placed into a common nuclear background, demonstrating that the benefits of rapamycin to mitochondrial metabolism depend on genes encoded in the mtDNA. Rapamycin is able to enhance mitochondrial respiration when succinate dehydrogenase activity is blocked, suggesting that the beneficial effects of rapamycin on these two processes are independent. Overall, this study provides the first evidence for a link between mitochondrial genotype and the effects of rapamycin on mitochondrial metabolic pathways.

Indexed as

AnimalsDNA, MitochondrialDown-RegulationDrosophila melanogasterFemaleMitochondriaOxidation-ReductionSirolimusTOR Serine-Threonine KinasesDNA, MitochondrialSirolimusTOR Serine-Threonine KinasesMetabolismMitochondrial genotypeRapamycin

Identifiers

PMID24610944
PMCPMC4021473
OpenAlexW2113095366

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.