ArticleThe Journal of biological chemistry2010
Neurologic dysfunction and male infertility in Drosophila porin mutants: a new model for mitochondrial dysfunction and disease.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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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.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Highly conserved shifts in ubiquitin-proteasome system (UPS) activity drive mitochondrial remodeling during quiescence.Nature communications · 2022Article
- Redox-Sensitive VDAC: A Possible Function as an Environmental Stress Sensor Revealed by Bioinformatic Analysis.Frontiers in physiology · 2021Article
- Variation in Mitochondria-Derived Transcript Levels Associated With DDT Resistance in the 91-R Strain of Drosophila melanogaster (Diptera: Drosophilidae).Journal of insect science (Online) · 2018Article
- TheDisease models & mechanisms · 2018Article
- The Krebs Cycle Enzyme Isocitrate Dehydrogenase 3A Couples Mitochondrial Metabolism to Synaptic Transmission.Cell reports · 2017Article
- Peroxisomal biogenesis is genetically and biochemically linked to carbohydrate metabolism in Drosophila and mouse.PLoS genetics · 2017Article
- Loss of porin function in dopaminergic neurons of Drosophila is suppressed by Buffy.Journal of biomedical science · 2016Article
- Preparation of purified perikaryal and synaptosomal mitochondrial fractions from relatively small hypothalamic brain samples.MethodsX · 2016Article
- Impaired Mitochondrial Energy Production Causes Light-Induced Photoreceptor Degeneration Independent of Oxidative Stress.PLoS biology · 2015Article
- Article
- Expression of alternative oxidase in Drosophila ameliorates diverse phenotypes due to cytochrome oxidase deficiency.Human molecular genetics · 2014Article
- Screen for abnormal mitochondrial phenotypes in mouse embryonic stem cells identifies a model for succinyl-CoA ligase deficiency and mtDNA depletion.Disease models & mechanisms · 2014Article
- Article
- Loss of mitochondrial peptidase Clpp leads to infertility, hearing loss plus growth retardation via accumulation of CLPX, mtDNA and inflammatory factors.Human molecular genetics · 2013Article
- The C8ORF38 homologue Sicily is a cytosolic chaperone for a mitochondrial complex I subunit.The Journal of cell biology · 2013Article
- Voltage-dependant anion channels: novel insights into isoform function through genetic models.Biochimica et biophysica acta · 2012Review
- Sox9 and NFIA coordinate a transcriptional regulatory cascade during the initiation of gliogenesis.Neuron · 2012Article
- Voltage-dependent-anion-channels (VDACs) in Arabidopsis have a dual localization in the cell but show a distinct role in mitochondria.Plant molecular biology · 2012Article
- The yeast complex I equivalent NADH dehydrogenase rescues pink1 mutants.PLoS genetics · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Voltage-dependent anion channels (VDACs) are a family of small pore-forming proteins of the mitochondrial outer membrane found in all eukaryotes. VDACs play an important role in the regulated flux of metabolites between the cytosolic and mitochondrial compartments, and three distinct mammalian isoforms have been identified. Animal and cell culture experiments suggest that the various isoforms act in disparate roles such as apoptosis, synaptic plasticity, learning, muscle bioenergetics, and reproduction. In Drosophila melanogaster, porin is the ubiquitously expressed VDAC isoform. Through imprecise excision of a P element insertion in the porin locus, a series of hypomorphic alleles have been isolated, and analyses of flies homozygous for these mutant alleles reveal phenotypes remarkably reminiscent of mouse VDAC mutants. These include partial lethality, defects of mitochondrial respiration, abnormal muscle mitochondrial morphology, synaptic dysfunction, and male infertility, which are features often observed in human mitochondrial disorders. Furthermore, the observed synaptic dysfunction at the neuromuscular junction in porin mutants is associated with a paucity of mitochondria in presynaptic termini. The similarity of VDAC mutant phenotypes in the fly and mouse clearly indicate a fundamental conservation of VDAC function. The establishment and validation of a new in vivo model for VDAC function in Drosophila should provide a valuable tool for further genetic dissection of VDAC role(s) in mitochondrial biology and disease, and as a model of mitochondrial disorders potentially amenable to the development of treatment strategies.
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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.