ArticlePloS one2013
Huntingtin's function in axonal transport is conserved in Drosophila melanogaster.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 58 citations in OpenAlex.
- Huntingtin and its allies at the cortico-striatal synapse.Cell death & disease · 2026Review
- Advances in gene and cellular therapeutic approaches for Huntington's disease.Protein & cell · 2025Review
- Disruption of axonal transport in neurodegeneration.The Journal of clinical investigation · 2023Review
- Huntingtin and Other Neurodegeneration-Associated Proteins in the Development of Intracellular Pathologies: Potential Target Search for Therapeutic Intervention.International journal of molecular sciences · 2022Review
- HAP40 is a conserved central regulator of Huntingtin and a potential modulator of Huntington's disease pathogenesis.PLoS genetics · 2022Article
- In Vivo Live Imaging of Axonal Transport in Developing Zebrafish Axons.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Huntingtin and the Synapse.Frontiers in cellular neuroscience · 2021Review
- Do Changes in Synaptic Autophagy Underlie the Cognitive Impairments in Huntington's Disease?Journal of Huntington's disease · 2021Review
- Proteotoxicity and Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Excess Rab4 rescues synaptic and behavioral dysfunction caused by defective HTT-Rab4 axonal transport in Huntington's disease.Acta neuropathologica communications · 2020Article
- Review
- Mutant Huntingtin affects toll-like receptor 4 intracellular trafficking and cytokine production in mast cells.Journal of neuroinflammation · 2020Article
- RNA Aptamers Rescue Mitochondrial Dysfunction in a Yeast Model of Huntington's Disease.Molecular therapy. Nucleic acids · 2018Article
- The TinyInternational journal of molecular sciences · 2018Review
- NOS3 Inhibition Confers Post-Ischemic Protection to Young and Aging White Matter Integrity by Conserving Mitochondrial Dynamics and Miro-2 Levels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Huntington's disease: the coming of age.Journal of genetics · 2018Review
- Mitochondrial dynamics and preconditioning in white matter.Conditioning medicine · 2018Article
- Loss of Huntingtin stimulates capture of retrograde dense-core vesicles to increase synaptic neuropeptide stores.European journal of cell biology · 2017Article
- Huntingtin Is Required for Neural But Not Cardiac/Pancreatic Progenitor Differentiation of Mouse Embryonic Stem CellsFrontiers in cellular neuroscience · 2017Article
- Lissencephaly-1 dependent axonal retrograde transport of L1-type CAM Neuroglian in the adult drosophila central nervous system.PloS one · 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a devastating dominantly inherited neurodegenerative disorder caused by an abnormal polyglutamine expansion in the N-terminal part of the huntingtin (HTT) protein. HTT is a large scaffold protein that interacts with more than a hundred proteins and is probably involved in several cellular functions. The mutation is dominant, and is thought to confer new and toxic functions to the protein. However, there is emerging evidence that the mutation also alters HTT's normal functions. Therefore, HD models need to recapitulate this duality if they are to be relevant. Drosophila melanogaster is a useful in vivo model, widely used to study HD through the overexpression of full-length or N-terminal fragments of mutant human HTT. However, it is unclear whether Drosophila huntingtin (DmHTT) shares functions similar to the mammalian HTT. Here, we used various complementary approaches to analyze the function of DmHTT in fast axonal transport. We show that DmHTT interacts with the molecular motor dynein, associates with vesicles and co-sediments with microtubules. DmHTT co-localizes with Brain-derived neurotrophic factor (BDNF)-containing vesicles in rat cortical neurons and partially replaces mammalian HTT in a fast axonal transport assay. DmHTT-KO flies show a reduced fast axonal transport of synaptotagmin vesicles in motoneurons in vivo. These results suggest that the function of HTT in axonal transport is conserved between flies and mammals. Our study therefore validates Drosophila melanogaster as a model to study HTT function, and its dysfunction associated with HD.
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.