ArticleGenetics2006
Post-transcriptional silencing and functional characterization of the Drosophila melanogaster homolog of human Surf1.
Article in Genetics, 2006. 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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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Disease models of Leigh syndrome: From yeast to organoids.Journal of inherited metabolic disease · 2024Review
- Mitochondrial Neurodegeneration: Lessons fromBiomolecules · 2023Review
- The function of Scox in glial cells is essential for locomotive ability in Drosophila.Scientific reports · 2021Article
- Lifelong reduction in complex IV induces tissue-specific metabolic effects but does not reduce lifespan or healthspan in mice.Aging cell · 2018Article
- Ras-ERK-ETS inhibition alleviates neuronal mitochondrial dysfunction by reprogramming mitochondrial retrograde signaling.PLoS genetics · 2018Article
- SURF1 knockout cloned pigs: Early onset of a severe lethal phenotype.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Mitonuclear communication in homeostasis and stress.Nature reviews. Molecular cell biology · 2016Review
- Mitochondrial cytochrome c oxidase deficiency.Clinical science (London, England : 1979) · 2016Review
- Mitochondrial retrograde signaling regulates neuronal function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Cardiac deficiency of single cytochrome oxidase assembly factor scox induces p53-dependent apoptosis in a Drosophila cardiomyopathy model.Human molecular genetics · 2015Article
- Mitochondrial Diseases Part I: mouse models of OXPHOS deficiencies caused by defects in respiratory complex subunits or assembly factors.Mitochondrion · 2015Review
- Leigh syndrome in Drosophila melanogaster: morphological and biochemical characterization of Surf1 post-transcriptional silencing.The Journal of biological chemistry · 2014Article
- Expression of alternative oxidase in Drosophila ameliorates diverse phenotypes due to cytochrome oxidase deficiency.Human molecular genetics · 2014Article
- Functional characterization of drim2, the Drosophila melanogaster homolog of the yeast mitochondrial deoxynucleotide transporter.The Journal of biological chemistry · 2014Article
- A mitocentric view of Parkinson's disease.Annual review of neuroscience · 2014Review
- The SFT-1 and OXA-1 respiratory chain complex assembly factors influence lifespan by distinct mechanisms in C. elegans.Longevity & healthspan · 2013Article
- Fly cryptochrome and the visual system.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- 2mit, an intronic gene of Drosophila melanogaster timeless2, is involved in behavioral plasticity.PloS one · 2013Article
- Mutations in TTC19 cause mitochondrial complex III deficiency and neurological impairment in humans and flies.Nature genetics · 2011Article
- Drosophila melanogaster as a model organism of brain diseases.International journal of molecular sciences · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in Surf1, a human gene involved in the assembly of cytochrome c oxidase (COX), cause Leigh syndrome, the most common infantile mitochondrial encephalopathy, characterized by a specific COX deficiency. We report the generation and characterization of functional knockdown (KD) lines for Surf1 in Drosophila. KD was produced by post-transcriptional silencing employing a transgene encoding a dsRNA fragment of the Drosophila homolog of human Surf1, activated by the UAS transcriptional activator. Two alternative drivers, Actin5C-GAL4 or elav-GAL4, were used to induce silencing ubiquitously or in the CNS, respectively. Actin5C-GAL4 KD produced 100% egg-to-adult lethality. Most individuals died as larvae, which were sluggish and small. The few larvae reaching the pupal stage died as early imagos. Electron microscopy of larval muscles showed severely altered mitochondria. elav-GAL4-driven KD individuals developed to adulthood, although cephalic sections revealed low COX-specific activity. Behavioral and electrophysiological abnormalities were detected, including reduced photoresponsiveness in KD larvae using either driver, reduced locomotor speed in Actin5C-GAL4 KD larvae, and impaired optomotor response as well as abnormal electroretinograms in elav-GAL4 KD flies. These results indicate important functions for SURF1 specifically related to COX activity and suggest a crucial role of mitochondrial energy pathways in organogenesis and CNS development and function.
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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.