ArticleGenetics2002
The Drosophila slamdance gene: a mutation in an aminopeptidase can cause seizure, paralysis and neuronal failure.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 100 citations in OpenAlex.
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- Pyridox (am) ine 5'-phosphate oxidase deficiency induces seizures in Drosophila melanogaster.Human molecular genetics · 2019Article
- Milk-whey diet substantially suppresses seizure-like phenotypes ofJournal of neurogenetics · 2019Article
- Alterations in Organismal Physiology, Impaired Stress Resistance, and Accelerated Aging inOxidative medicine and cellular longevity · 2019Article
- Shortened Lifespan and Other Age-Related Defects in Bang Sensitive Mutants ofG3 (Bethesda, Md.) · 2018Article
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- Seizure control through genetic and pharmacological manipulation of Pumilio in Drosophila: a key component of neuronal homeostasis.Disease models & mechanisms · 2017Article
- Seizure Suppression by High Temperature via cAMP Modulation in Drosophila.G3 (Bethesda, Md.) · 2016Article
- Mutation of orthologous prickle genes causes a similar epilepsy syndrome in flies and humans.Annals of clinical and translational neurology · 2016Article
- Mutations of the Calcium Channel Gene cacophony Suppress Seizures in Drosophila.PLoS genetics · 2016Article
- Drosophila sodium channel mutations: Contributions to seizure-susceptibility.Experimental neurology · 2015Review
- Drosophila Nipped-B Mutants Model Cornelia de Lange Syndrome in Growth and Behavior.PLoS genetics · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report here the characterization of slamdance (sda), a Drosophila melanogaster "bang-sensitive" (BS) paralytic mutant. This mutant exhibits hyperactive behavior and paralysis following a mechanical "bang" or electrical shock. Electrophysiological analyses have shown that this mutant is much more prone to seizure episodes than normal flies because it has a drastically lowered seizure threshold. Through genetic mapping, molecular cloning, and RNA interference, we have demonstrated that the sda phenotype can be attributed to a mutation in the Drosophila homolog of the human aminopeptidase N (APN) gene. Furthermore, using mRNA in situ hybridization and LacZ staining, we have found that the sda gene is expressed specifically in the central nervous system at particular developmental stages. Together, these results suggest that the bang sensitivity in sda mutants is caused by a defective APN gene that somehow increases seizure susceptibility. Finally, by using the sda mutation as a sensitized background, we have been able to identify a rich variety of sda enhancers and other independent BS mutations.
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