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General Information
Symbol
Dmel\cacS
Species
D. melanogaster
Name
FlyBase ID
FBal0091230
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    point mutation
    Nucleotide change:

    T11964153A

    Reported nucleotide change:

    T?A

    Amino acid change:

    F1029I | cac-PA; F1029I | cac-PB; F1029I | cac-PC; F1029I | cac-PD; F1029I | cac-PE; F1029I | cac-PF; F1029I | cac-PG; F1029I | cac-PH; F1029I | cac-PI; F1029I | cac-PJ; F1029I | cac-PL; F1029I | cac-PM; F1135I | cac-PN; F1029I | cac-PO; F1029I | cac-PP

    Reported amino acid change:

    F?I

    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Amino acid replacement: F?I.

    Transversion in the sequence encoding transmembrane domain IIIS6. This would be expected to affect all splice variants. The altered F residue is perfectly conserved in calcium channel α1 and sodium channel α subunits and some potassium channel subunits.

    Nucleotide substitution: T?A.

    Expression Data
    Reporter Expression
    Additional Information
    Statement
    Reference
     
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 0 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference

    cacS mutants exhibit a dramatic reduction in air puff-triggered flight initiation success. However, these flies display spontaneous sustained flight, with significantly increased wing beat frequency coupled with higher DLM firing rates well beyond the maximum firing frequency found in wild-type flies. There is a subtle yet statistically significant increase in the CV for cacS mutant flies.

    cacS homozygotes and cacS/cacNT27 trans-heterozygotes exhibit an increase in type M satellites (small boutons).

    Heterozygous larvae show reduced synaptic homeostasis at the neuromuscular junction after treatment with philanthotoxin-433 compared to control larvae.

    cacS heterozygosity has no effect on the rapid induction of homeostatic signaling at the neuromuscular junction (NMJ) following philanthatoxin (PhTx) application.

    Heterozygous, homozygous and cacS/cacTS2 P1 stage pupae have a significantly increased heart rate and an increased strength of heart beat rhythmicity compared to controls.

    Duration of copulation in mutant males is about 30% longer than in wild-type males. Analysis of the average numbers of intrapulse cycles (CPP) per song bout of reasonable length indicates that at 20oC and 30oC mutant males generate song pulses containing larger than normal numbers of cycles.

    At 36oC, mutant flies show spinning behaviour and a lack of coordination. At 36oC, 50% of homozygotes show paralysis in 39.57 +/- 1.25 minutes. At 38oC, 50% of homozygotes show paralysis in 19.97 +/- 1.78 minutes.

    Mutants show a reduction in the synaptic current at the dorsal longitudinal flight muscle (DLM) neuromuscular synapse compared to wild type. The decrease in the synaptic current is activity-dependent and shows no clear dependence on temperature.

    General characteristics of mutant phenotype: Song pulse - mutant; Optomotor test - wild-type; CC-phototaxis - wild-type; Y-phototaxis - wild-type; ERG transients - wild-type; ERG LCRP amplitude - wild-type; ERG LCRP kinetics - wild-type; ERG Rebound - mutant; ERG refractory wandering - wild-type.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    Statement
    Reference

    GluRIIASP16, cacS/cac[+] has neurophysiology defective phenotype, enhanceable by Csp[+]/CspDG29203

    NOT Enhanced by
    Statement
    Reference

    cacS has neurophysiology defective | dominant phenotype, non-enhanceable by CG6856[+]/Dysbe01028

    Enhancer of
    Statement
    Reference

    cacS is an enhancer of paralytic | heat sensitive phenotype of comt4

    Suppressor of
    Statement
    Reference

    cacS is a suppressor of neuroanatomy defective phenotype of sei2

    cacS/cacNT27 is a suppressor of neuroanatomy defective phenotype of sei2

    Other
    Phenotype Manifest In
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    GluRIIASP16/GluRIIASP16;cacS/+ third instar larvae show significant decreases in mEPSP (decreasing quantal size) and partial impairment of compensatory homeostatic increases in quantal content (significantly less quantal content than is seen in GluRIIASP16/GluRIIASP16 mutants alone but significantly more than wild type) at the NMJ. GluRIIASP16/GluRIIASP16 cacS/+ Cskj1D8/+ third instar larvae show significant decreases in mEPSP and quantal content at the NMJ.

    The NMJs of cacS GluRIIASP16 double mutant larvae exhibit partially impaired synaptic homeostasis.

    One copy of CspDG29203 prevents the compensatory increase in quantal content seen in the NMJs of cacS/+; GluRIIASP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with cacS/+; CspDG29203/+ controls.

    A cacS or cacS/cacNT27 background suppresses satellite frequency in sei2 mutants. Double mutants display a drastic decrease in both type B and M satellites, along with an even more pronounced reduction in the number of mature boutons and terminal branches.

    A cacS background suppresses satellite frequency in slo1, slo4 and slo98 mutants.

    The phenotype of reduced synaptic homeostasis at the neuromuscular junction after treatment with philanthotoxin-433 that is seen in cacS/+ larvae is not enhanced by dysbe01028/+.

    The heterozygous cacS/+ mutation mildly suppresses, but does not abolish the synaptic homeostatic compensation response at the neuromuscular junction (NMJ) seen in homozygous GluRIIASP16 single mutants.

    The recessive GluRIIASP16 single mutant NMJ synaptic homeostasis phenotype is completely suppressed in the presence of a heterozygous cacS mutation in combination with either an ExnEY01953 or an ExnEY-Δ23 heterozygous genetic background.

    cacS/+; ; ExnEY01953/+ double heterozygotes show a severe disruption of the rapid induction of homeostatic signaling at the neuromuscular junction following philanthatoxin (PhTx) application.

    The combination of Rac1J11/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

    The combination of Rho172O/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

    The combination of Cdc423/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

    cacS comt4 double mutants show faster paralysis than comt4 single mutants at both 36o and 38oC.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Fails to complement
    Comments

    cacTS2 complements the cacS phenotype at 20oC but fails to complement it at 36oC.

    Extensive phenogenetic analysis of allelic combinations reveals a phenotypic series for visually mediated behaviors and genetically separable ERG defects and courtship song defects.

    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (3)
    References (14)