Evidence map›Paper›PMID 36266680›Full record

ArticleBMC biology2022

orsai, the Drosophila homolog of human ETFRF1, links lipid catabolism to growth control.

Magdalena Fernandez-Acosta, Juan I Romero, Guillermo Bernabó, Giovanna M Velázquez-Campos, Nerina Gonzalez, M Lucía Mares, Santiago Werbajh, L Amaranta Avendaño-Vázquez, Gerald N Rechberger, Ronald P Kühnlein and 4 more

Open access · goldAbstract read
In one paragraph

Article in BMC biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
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

14 authors at 3 institutions in 5 countries.

Magdalena Fernandez-Acosta *Laboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.ORCID 0000-0001-7850-0257
Juan I Romero *Laboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.ORCID 0000-0003-2323-0864
Guillermo Bernabó *Laboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
Giovanna M Velázquez-CamposLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
Nerina GonzalezLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
M Lucía MaresLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
Santiago WerbajhLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
L Amaranta Avendaño-VázquezLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.
Gerald N RechbergerInstitute for Molecular Biosciences, University of Graz, Graz, Austria.ORCID 0000-0002-0071-317X
Ronald P KühnleinInstitute for Molecular Biosciences, University of Graz, Graz, Austria.ORCID 0000-0003-1448-4117
Cristina Marino-BusljeLaboratorio de Bioinformática Estructural, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.ORCID 0000-0002-6564-1920
Rafael CanteraDepartamento de Biología del Neurodesarrollo, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay.
Carolina RezavalLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina.ORCID 0000-0002-1410-5589
M Fernanda CerianiLaboratorio de Genética del Comportamiento, Fundación Instituto Leloir - Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA- CONICET), Buenos Aires, Argentina. fceriani@leloir.org.ar.ORCID 0000-0001-8945-3070
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Graz · ATStockholm University · SE

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
NIH HHS P40 OD018537
6 · The paper itself

Abstract

backgroundLipid homeostasis is an evolutionarily conserved process that is crucial for energy production, storage and consumption. Drosophila larvae feed continuously to achieve the roughly 200-fold increase in size and accumulate sufficient reserves to provide all energy and nutrients necessary for the development of the adult fly. The mechanisms controlling this metabolic program are poorly understood.

resultsHerein we identified a highly conserved gene, orsai (osi), as a key player in lipid metabolism in Drosophila. Lack of osi function in the larval fat body, the regulatory hub of lipid homeostasis, reduces lipid reserves and energy output, evidenced by decreased ATP production and increased ROS levels. Metabolic defects due to reduced Orsai (Osi) in time trigger defective food-seeking behavior and lethality. Further, we demonstrate that downregulation of Lipase 3, a fat body-specific lipase involved in lipid catabolism in response to starvation, rescues the reduced lipid droplet size associated with defective orsai. Finally, we show that osi-related phenotypes are rescued through the expression of its human ortholog ETFRF1/LYRm5, known to modulate the entry of β-oxidation products into the electron transport chain; moreover, knocking down electron transport flavoproteins EtfQ0 and walrus/ETFA rescues osi-related phenotypes, further supporting this mode of action.

conclusionsThese findings suggest that Osi may act in concert with the ETF complex to coordinate lipid homeostasis in the fat body in response to stage-specific demands, supporting cellular functions that in turn result in an adaptive behavioral response.

Indexed as

Drosophila melanogasterDrosophila ProteinsLipid MetabolismAdenosine TriphosphateAnimalsFat BodyFlavoproteinsHumansLarvaLipaseLipidsReactive Oxygen SpeciesAdenosine TriphosphateDrosophila ProteinsFlavoproteinsLipaseLipidsReactive Oxygen SpeciesCG6115Drosophila melanogasterETFRF1Fat bodyLipid dropletsLipid metabolismLYR

Identifiers

PMID36266680
PMCPMC9585818
OpenAlexW4306920812

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.