A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\KCNQ186

General Information
SymbolDmel\KCNQ186SpeciesD. melanogaster
NameFlyBase IDFBal0244108
Feature typealleleAssociated geneDmel\KCNQ
Allele class
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
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Associated Sequence Data
DDBJ /
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DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
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Progenitor genotype
Nature of the lesion
Statement
Reference
Imprecise excision of the progenitor insertion, deleting all transmembrane domains including the potassium selective pore region of the KCNQ channel.
Cytology
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Statement
Reference
KCNQ[186] mutant larvae take 1-2 days longer to develop, a reduced number of animals eclose, and the mean lifespan of females is reduced by 20-30%. Mutant adults show a drastically increased incidence of pacing-induced cardiac dysfunction compared to age-matched controls, and the elevated failure rates observed in young mutant flies does not increase further with age. Semi-intact KCNQ[186] fly heart preparations from young (1-3 week old) flies exhibit severely nonrhythmic beating patterns, and the incidence of arrhythmia increases more rapidly with age compared to control preparations. A dramatic age-dependent increase of the heart period (defined as the length of time between the ends of two consecutive diastolic intervals) compared with age-matched controls is also observed, and both diastolic intervals and systolic intervals show age-dependent increases in length. Electrophysiology field potential recordings from semi-intact KCNQ[186] fly heart preparations show that negative deflections do not immediately follow the initial positive potentials, and usually occur with significant delay compared to wildtype preparations. Semi-intact KCNQ[186] fly heart preparations show lower rates of muscle contractions compared to controls. In response to electrical stimulation, hearts exhibit fibrillation, markedly elevated diastolic tension, and extremely delayed recovery to baseline diastolic tension relative to wildtype hearts.
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Rescued by
Comments
Expression of KCNQ[Scer\UAS.cOa] under the control of Scer\GAL4[how-24B] in a KCNQ[186] mutant background rescues the increased pacer-induced cardiac dysfunction rates and alterations in rhythmicity to levels comparable to those observed in control animals.
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Research paper
Fabrizio et al., 2012, Fly 6(4): 261--272
mulet (mlt) encodes a tubulin-binding cofactor E-like homolog required for spermatid individualization in Drosophila melanogaster. [FBrf0220242]
Ocorr et al., 2007, Proc. Natl. Acad. Sci. U.S.A. 104(10): 3943--3948
KCNQ potassium channel mutations cause cardiac arrhythmias in Drosophila that mimic the effects of aging. [FBrf0193190]