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General Information
Name
seizure-sensitivity model, Dmel\jus
FlyBase ID
FBhh0000314
Disease Ontology Term
Parent Disease
OMIM
Overview

Mutations in a number of Drosophila genes produce phenotypes of seizure sensitivity, including a lowered threshold to evoked electrophysiologically recorded seizure-like activity and "bang-sensitive" phenotypes. This report describes work done with the fly gene jus (julius seizure; originally designated slamdance, sda). Dmel\jus encodes a novel transmembrane protein containing two transmembrane domains and an extracellular cysteine-rich loop. Classical loss-of-function alleles, RNAi-targeting constructs, and alleles caused by insertional mutagenesis have been generated for jus. No human gene orthologous to Dmel\jus has been identified.

Dmel\jus adults exhibit strong seizure-sensitive phenotypes, including cold-sensitive paralysis and partial sensitivity to strobe-induced seizures. RNAi directed to different cell types has established that jus is required in neurons but not glia; partial bang-sensitivity is caused by knockdown in GABAergic or cholinergic but not glutamatergic neurons. A large number of genetic interactions have been described for this gene; see the gene report for jus.

[updated Oct. 2018 by FlyBase; FBrf0222196]

Disease Summary Information
Disease Summary: seizure-sensitivity model, Dmel\jus
OMIM report
Human gene(s) implicated
Symptoms and phenotype
Genetics
Cellular phenotype and pathology
Molecular information
External links
    Disease synonyms
    seizure-sensitive (postulated), Dmel\jus-related
    seizure-sensitive (postulated), Dmel\sda-related
    seizure sensitivity
    Ortholog Information
    Human gene(s) in FlyBase
      Other mammalian ortholog(s) used
        D. melanogaster Gene Information (1)
        Gene Snapshot
        julius seizure (jus) encodes a two-transmembrane domain protein expressed in selected neurons in the optic lobe, subesophageal and thoracic-abdominal ganglia. It is mainly localized to axons and its developmental expression prevents epileptogenesis. [Date last reviewed: 2018-11-08]
        Molecular function (GO)
          Cellular component (GO)
            Gene Groups / Pathways
              Comments on ortholog(s)

              No identified orthologous genes in human.

              Orthologs and Alignments from DRSC
              DIOPT - DRSC Integrative Ortholog Prediction Tool - Click the link below to search for orthologs in Humans
              Other Genes Used: Viral, Bacterial, Synthetic (0)
                Summary of Physical Interactions (0 groups)
                Alleles Reported to Model Human Disease (Disease Ontology) (5 alleles)
                Models Based on Experimental Evidence ( 5 )
                Modifiers Based on Experimental Evidence ( 1 )
                Allele
                Disease
                Interaction
                References
                model of  epilepsy
                is ameliorated by shi1
                is ameliorated by shi2
                Alleles Representing Disease-Implicated Variants
                Genetic Tools, Stocks and Reagents
                Sources of Stocks
                Contact lab of origin for a reagent not available from a public stock center.
                Bloomington Stock Center Disease Page
                Selected mammalian transgenes
                Allele
                Transgene
                Publicly Available Stocks
                Selected Drosophila transgenes
                Allele
                Transgene
                Publicly Available Stocks
                RNAi constructs available
                Allele
                Transgene
                Publicly Available Stocks
                Selected Drosophila classical alleles
                Allele
                Allele class
                Mutagen
                Publicly Available Stocks
                phiC31 integrase
                spontaneous
                References (21)