FlyBase Allele Report: Dmel\cac[S]

General Information

Symbol

Dmel\cac^S

Species

D. melanogaster

Name

FlyBase ID

FBal0091230

Feature type

allele

Associated gene

Dmel\cac

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Amino acid replacement: F?I.

(Smith et al., 1998)

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.

(Smith et al., 1998)

Nucleotide substitution: T?A.

(Smith et al., 1998)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:11,964,153..11,964,153 [-]

Nucleotide change:

T11964153A

Reported nucleotide change:

T?A

Amino acid change:

Reported amino acid change:

F?I

(Smith et al., 1998)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

dorsal medial muscle & synapse

(Kawasaki et al., 2000)

NMJ bouton | increased number

(Lee and Wu, 2010)

NMJ bouton | increased number (with cac^NT27)

(Lee and Wu, 2010)

Detailed Description

Statement

Reference

cac^S 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 cac^S mutant flies.

(Iyengar and Wu, 2014)

cac^S homozygotes and cac^S/cac^NT27 trans-heterozygotes exhibit an increase in type M satellites (small boutons).

(Lee and Wu, 2010)

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

(Dickman and Davis, 2009)

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

(Frank et al., 2009)

Heterozygous, homozygous and cac^S/cac^TS2 P1 stage pupae have a significantly increased heart rate and an increased strength of heart beat rhythmicity compared to controls.

(Ray and Dowse, 2005)

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 20^oC and 30^oC mutant males generate song pulses containing larger than normal numbers of cycles.

(Chan et al., 2002)

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

(Dellinger et al., 2000)

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.

(Kawasaki et al., 2000)

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.

(Smith et al., 1998)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology phenotype, enhanceable by Csp[+]/Csp^DG29203

(Brusich et al., 2015)

NOT Enhanced by

Statement

Reference

cac^S has abnormal neurophysiology | dominant phenotype, non-enhanceable by CG6856[+]/Dysb^e01028

(Dickman and Davis, 2009)

Enhancer of

Statement

Reference

cac^S is an enhancer of paralytic | heat sensitive phenotype of comt⁴

(Dellinger et al., 2000)

Suppressor of

Statement

Reference

cac^S is a suppressor of abnormal neuroanatomy phenotype of sei²

(Lee and Wu, 2010)

cac^S/cac^NT27 is a suppressor of abnormal neuroanatomy phenotype of sei²

(Lee and Wu, 2010)

Other

Statement

Reference

Csk^j1D8/Csk[+], GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | third instar larval stage phenotype

(Spring et al., 2016)

GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | third instar larval stage phenotype

(Spring et al., 2016)

GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology phenotype

(Brusich et al., 2015)

GluRIIA^SP16, Rac1^J11/Rac1[+], cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Cdc42[+]/Cdc42³, GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Exn^EY-Δ23, GluRIIA^SP16, cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Phenotype Manifest In

Suppressor of

Statement

Reference

cac^S is a suppressor of NMJ bouton | increased number phenotype of sei²

(Lee and Wu, 2010)

cac^S is a suppressor of neuromuscular junction phenotype of sei²

(Lee and Wu, 2010)

cac^S/cac^NT27 is a suppressor of NMJ bouton | increased number phenotype of sei²

(Lee and Wu, 2010)

cac^S/cac^NT27 is a suppressor of neuromuscular junction phenotype of sei²

(Lee and Wu, 2010)

Other

Statement

Reference

Csk^j1D8/Csk[+], GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Spring et al., 2016)

GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction | third instar larval stage phenotype

(Spring et al., 2016)

GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Cdc42[+]/Cdc42³, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Exn^EY01953, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Exn^EY-Δ23, GluRIIA^SP16, cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

GluRIIA^SP16, Rac1^J11/Rac1[+], cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

GluRIIA^SP16/GluRIIA^SP16;cac^S/+ 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 GluRIIA^SP16/GluRIIA^SP16 mutants alone but significantly more than wild type) at the NMJ. GluRIIA^SP16/GluRIIA^SP16 cac^S/+ Csk^j1D8/+ third instar larvae show significant decreases in mEPSP and quantal content at the NMJ.

(Spring et al., 2016)

The NMJs of cac^S GluRIIA^SP16 double mutant larvae exhibit partially impaired synaptic homeostasis.

One copy of Csp^DG29203 prevents the compensatory increase in quantal content seen in the NMJs of cac^S/+; GluRIIA^SP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with cac^S/+; Csp^DG29203/+ controls.

(Brusich et al., 2015)

A cac^S or cac^S/cac^NT27 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 cac^S background suppresses satellite frequency in slo¹, slo⁴ and slo⁹⁸ mutants.

(Lee and Wu, 2010)

The phenotype of reduced synaptic homeostasis at the neuromuscular junction after treatment with philanthotoxin-433 that is seen in cac^S/+ larvae is not enhanced by dysb^e01028/+.

(Dickman and Davis, 2009)

The heterozygous cac^S/+ mutation mildly suppresses, but does not abolish the synaptic homeostatic compensation response at the neuromuscular junction (NMJ) seen in homozygous GluRIIA^SP16 single mutants.

The recessive GluRIIA^SP16 single mutant NMJ synaptic homeostasis phenotype is completely suppressed in the presence of a heterozygous cac^S mutation in combination with either an Exn^EY01953 or an Exn^EY-Δ23 heterozygous genetic background.

cac^S/+; ; Exn^EY01953/+ double heterozygotes show a severe disruption of the rapid induction of homeostatic signaling at the neuromuscular junction following philanthatoxin (PhTx) application.

The combination of Rac1^J11/+ and cac^S/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA^SP16 genetic background.

The combination of Rho1^72O/+ and cac^S/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA^SP16 genetic background.

The combination of Cdc42³/+ and cac^S/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA^SP16 genetic background.

(Frank et al., 2009)

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

(Dellinger et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

cac^TS2

(Dellinger et al., 2000)

Comments

cac^TS2 complements the cac^S phenotype at 20^oC but fails to complement it at 36^oC.

(Kawasaki et al., 2000)

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

(Smith et al., 1998)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

cac^S

(Limpitikul et al., 2018, Spring et al., 2016, Terada et al., 2016, Brusich et al., 2015, Gaviño et al., 2015, Iyengar and Wu, 2014, Dickman and Davis, 2009, Frank et al., 2009, Ray and Dowse, 2005)

cac^s

(Wentzel et al., 2018, Lee and Wu, 2010, Yamamoto and Nakano, 1999)

nbA^S

Name Synonyms

Secondary FlyBase IDs

References (16)

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