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General Information
Symbol
Dmel\Trpγ1
Species
D. melanogaster
Name
FlyBase ID
FBal0240386
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
deletion
Comment:

A deletion generated by homologous recombination. Deletion extent determined from primer sequences.

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

Deletion removing 155 nucleotides from Trpγ1 exon 8. This removes sequence encoding amino acid residues 605-656. (Revision of data reported in FBrf0228530).

Insertion components
TI{TI}Trpγ1
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

Trpγ1 mutant adults show normal preference for less solid sucrose-agarose food than a harder one (higher agarose conc., same sucrose content) one in a two-way food choice assay.

Adult mutant males and females show significantly decreased locomotor activity compared to wild type (both average daily activity and peak activity are reduced). The flies also show a small but significant defect in negative geotaxis.

Mutant flies require four times as long as wild-type flies to complete the righting reflect.

Mutant flies show significantly reduced speed and precision of movements during walking compared to controls.

Homozygous and TrpγG4/Trpγ1 flies initiate crossing of gaps at a frequency similar to controls, but their ability to successfully traverse larger gaps is impaired compared to wild type. The defect in homozygous is due to an inability to perform all the normal fine postural adjustments while attempting to cross the gap.

Homozygous and TrpγG4/Trpγ1 tibial extensor muscles show a significant reduction in the action potential frequency in response to tibia deflections compared to controls.

The gustatory aversion of mutant flies to 6mM camphor in a two way-choice test is not significantly different from that seen in wild-type flies.

Mutant flies exhibit the wild type avoidance of aristolochic acid in food choice assays.

Mutant adults show normal avoidance of 1% citronellal in a direct airborne repellent test (DART) assay.

Mutant third instar larvae show a slight, but statistically insignificant decrease in the preference for 17.5[o]C over 14[o]C in a two-way choice test compared to wild-type controls.

trpγ1 mutants retain a preference for 18[o]C (i.e. are thermotactic).

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

Trpγ1 has uncoordinated | adult stage phenotype, suppressible by CalxB

Suppressor of
Statement
Reference

Trpγ1 is a suppressor of uncoordinated | adult stage phenotype of CalxB

Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Double mutant Trpγ1 ; CalxB flies have a significantly less severe defect in their ability to successfully traverse large gaps of 3.5mm compared to either single mutant.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

TrpγCH322-162M11 rescues defects in fine motor coordination which are seen in Trpγ1 flies.

TrpγCH322-162M11 rescues the action potential frequency of tibial extensor muscles in response to tibia deflections to wild type in Trpγ1 flies.

Expression of TrpγScer\UAS.cAa under the control of Scer\GAL4iav.PU, but not Scer\GAL4nompC.PP, in Trpγ1 flies rescues the action potential frequency of tibial extensor muscles in response to tibia deflections to wild type.

Expression of TrpγScer\UAS.cAa under the control of Scer\GAL4Trpγ-G4 in TrpγG4/Trpγ1 flies rescues the action potential frequency of tibial extensor muscles in response to tibia deflections to wild type and also rescues their ability to successfully traverse large gaps of 3.5mm to wild-type levels.

Expression of TrpγScer\UAS.cAa under the control of either Scer\GAL4elav.PU or Scer\GAL4iav.PU (neuronal drivers) rescues the reduced ability of Trpγ1 flies to successfully traverse large gaps of 3.5mm compared to controls. The defect is partially rescued if TrpγScer\UAS.cAa expression is driven by Scer\GAL4nompA.cK.

The vacuolar volume of the scolopale cells of the chordotonal organs is reduced compared to wild-type in homozygous animals. Other morphological features of the mutant scolopidia appear ultrastructurally normal.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (10)