ArticleDisease models & mechanisms2015
Clueless, a protein required for mitochondrial function, interacts with the PINK1-Parkin complex in Drosophila.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 51 citations in OpenAlex.
- RNAi-based screen for pigmentation iniScience · 2026Article
- Article
- Phosphoproteomic Profiling Reveals Overlapping and Distinct Signaling Pathways inbioRxiv : the preprint server for biology · 2025Article
- RNAi-based screen for pigmentation inbioRxiv : the preprint server for biology · 2025Article
- Mitochondrial proteases and their roles in mitophagy in plants, animals, and yeast.Plant & cell physiology · 2025Review
- Drosophila Clu ribonucleoprotein particle dynamics rely on the availability of functional Clu and translating ribosomes.Journal of cell science · 2025Article
- Prophylactically Feeding Manganese toAntioxidants (Basel, Switzerland) · 2025Article
- CLUH maintains functional mitochondria and translation in motoneuronal axons and prevents peripheral neuropathy.Science advances · 2024Article
- Mitochondrial Differentiation during Spermatogenesis: Lessons fromInternational journal of molecular sciences · 2024Review
- Elimination of virus-like particles reduces protein aggregation and extends replicative lifespan inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- LARP4 is an RNA-binding protein that binds nuclear-encoded mitochondrial mRNAs to promote mitochondrial function.RNA (New York, N.Y.) · 2024Article
- Nutrient-dependent regulation of a stable intron modulates germline mitochondrial quality control.Nature communications · 2024Article
- CLUH functions as a negative regulator of inflammation in human macrophages and determines ulcerative colitis pathogenesis.JCI insight · 2023Article
- Endogenous TOM20 Proximity Labeling: A Swiss-Knife for the Study of Mitochondrial Proteins in Human Cells.International journal of molecular sciences · 2023Article
- Mechanisms of mitochondrial respiratory adaptation.Nature reviews. Molecular cell biology · 2022Review
- Combined Effects of Different Alleles ofPlants (Basel, Switzerland) · 2022Article
- Plant mitochondrial FMT and its mammalian homolog CLUH controls development and behavior in Arabidopsis and locomotion in mice.Cellular and molecular life sciences : CMLS · 2022Article
- Clueless/CLUH regulates mitochondrial fission by promoting recruitment of Drp1 to mitochondria.Nature communications · 2022Article
- Loss of Drosophila Clueless differentially affects the mitochondrial proteome compared to loss of Sod2 and Pink1.Frontiers in physiology · 2022Article
- Visualizing the Effects of Oxidative Damage on Drosophila Egg Chambers using Live Imaging.Journal of visualized experiments : JoVE · 2021Article
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 at 2 institutions in 1 country.
Funding
Abstract
Loss of mitochondrial function often leads to neurodegeneration and is thought to be one of the underlying causes of neurodegenerative diseases such as Parkinson's disease (PD). However, the precise events linking mitochondrial dysfunction to neuronal death remain elusive. PTEN-induced putative kinase 1 (PINK1) and Parkin (Park), either of which, when mutated, are responsible for early-onset PD, mark individual mitochondria for destruction at the mitochondrial outer membrane. The specific molecular pathways that regulate signaling between the nucleus and mitochondria to sense mitochondrial dysfunction under normal physiological conditions are not well understood. Here, we show that Drosophila Clueless (Clu), a highly conserved protein required for normal mitochondrial function, can associate with Translocase of the outer membrane (TOM) 20, Porin and PINK1, and is thus located at the mitochondrial outer membrane. Previously, we found that clu genetically interacts with park in Drosophila female germ cells. Here, we show that clu also genetically interacts with PINK1, and our epistasis analysis places clu downstream of PINK1 and upstream of park. In addition, Clu forms a complex with PINK1 and Park, further supporting that Clu links mitochondrial function with the PINK1-Park pathway. Lack of Clu causes PINK1 and Park to interact with each other, and clu mutants have decreased mitochondrial protein levels, suggesting that Clu can act as a negative regulator of the PINK1-Park pathway. Taken together, these results suggest that Clu directly modulates mitochondrial function, and that Clu's function contributes to the PINK1-Park pathway of mitochondrial quality control.
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.