ArticlePloS one2009
Nutrition controls mitochondrial biogenesis in the Drosophila adipose tissue through Delg and cyclin D/Cdk4.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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.
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.
Who cites it
33 citing papers in PubMed.
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- Altered mitochondrial functionality in metabolic disorders: insights fromFrontiers in endocrinology · 2026Review
- Control of mitochondrial dynamics by the metabolic regulator dPGC1 limits Yorkie-induced oncogenic growth in Drosophila.PLoS biology · 2025Article
- Effects of nutrients and diet on mitochondrial dysfunction: An opportunity for therapeutic approaches in human disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Impaired mitochondria-initiated crosstalk with lysosomes reciprocally aggravates mitochondrial defect through LManVI.Nature communications · 2025Article
- Interaction between neuromuscular junction metabolic requirements in fragile X syndrome and glycogen storage disease models.Disease models & mechanisms · 2025Article
- M1BP is an essential transcriptional activator of oxidative metabolism during Drosophila development.Nature communications · 2023Article
- Progressive transcriptional changes in metabolic genes and altered fatbody homeostasis in Drosophila model of Huntington's disease.Metabolic brain disease · 2022Article
- EGFR signaling activates intestinal stem cells by promoting mitochondrial biogenesis and β-oxidation.Current biology : CB · 2022Article
- Differential Proteomics Analysis Unraveled Mechanisms ofInsects · 2022Article
- An assessment of the rescue action of resveratrol in parkin loss of function-induced oxidative stress in Drosophila melanogaster.Scientific reports · 2022Article
- A cis-regulatory element promoting increased transcription at low temperature in cultured ectothermic Drosophila cells.BMC genomics · 2021Article
- Adipose triglyceride lipase protects renal cell endocytosis in a Drosophila dietary model of chronic kidney disease.PLoS biology · 2021Article
- Heterogeneity of Metabolic Vulnerability in Imatinib -Resistant Gastrointestinal Stromal Tumor.Cells · 2020Article
- PARIS induced defects in mitochondrial biogenesis drive dopamine neuron loss under conditions of parkin or PINK1 deficiency.Molecular neurodegeneration · 2020Article
- Role of cell cycle regulators in adipose tissue and whole body energy homeostasis.Cellular and molecular life sciences : CMLS · 2018Review
- Fueling the Cycle: CDKs in Carbon and Energy Metabolism.Frontiers in cell and developmental biology · 2018Review
- Loss of p16Oncotarget · 2017Article
- High-sucrose-induced maternal obesity disrupts ovarian function and decreases fertility in Drosophila melanogaster.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- A Molecular and Cellular Context-Dependent Role for Ir76b in Detection of Amino Acid Taste.Cell reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mitochondria are cellular organelles that perform critical metabolic functionsthey generate energy from nutrients but also provide metabolites for de novo synthesis of fatty acids and several amino acids. Thus mitochondrial mass and activity must be coordinated with nutrient availability, yet this remains poorly understood. Here, we demonstrate that Drosophila larvae grown in low yeast food have strong defects in mitochondrial abundance and respiration activity in the larval fat body. This correlates with reduced expression of genes encoding mitochondrial proteins, particularly genes involved in oxidative phosphorylation. Second, genes involved in glutamine metabolism are also expressed in a nutrient-dependent manner, suggesting a coordination of amino acid synthesis with mitochondrial abundance and activity. Moreover, we show that Delg (CG6338), the Drosophila homologue to the alpha subunit of mammalian transcription factor NRF-2/GABP, is required for proper expression of most genes encoding mitochondrial proteins. Our data demonstrate that Delg is critical to adjust mitochondrial abundance in respect to Cyclin D/Cdk4, a growth-promoting complex and glutamine metabolism according to nutrient availability. However, in contrast to nutrients, Delg is not involved in the regulation of mitochondrial activity in the fat body. These findings are the first genetic evidence that the regulation of mitochondrial mass can be uncoupled from mitochondrial activity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.