FB2025_01 , released February 20, 2025
Allele: Dmel\CalxB
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General Information
Symbol
Dmel\CalxB
Species
D. melanogaster
Name
FlyBase ID
FBal0193745
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

There is no mutation in the coding region of CalxB. There may be a mutation on a regulatory region.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
Detailed Description
Statement
Reference

Mutant flies have a significantly reduced ability to successfully traverse large gaps of 3.5mm compared to

A CalxB mutant background partially suppresses the degeneration of photoreceptors found when Sk2Scer\UAS.cYa is overexpressed in the developing eye under the control of Scer\GAL4GMR.PF.

Mutant flies have an abnormal electroretinogram (ERG); the light response terminates more rapidly than in wild-type flies.

Mutant flies show degeneration of rhabdomeres; when maintained under a 12 hour light-12 hour dark cycle almost all rhabdomeres have degenerated by 14 days after eclosion.

CalxB flies show a photoresponse inactivation phenotype.

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

CalxB has uncoordinated | adult stage phenotype, suppressible by Trpγ1

CalxB has abnormal neuroanatomy phenotype, suppressible by trp14

CalxB has abnormal neuroanatomy phenotype, suppressible by trp9

Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressed by
Statement
Reference

CalxB has rhabdomere phenotype, suppressible by trp14

CalxB has rhabdomere phenotype, suppressible by trp9

Suppressor of
Statement
Reference
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.

CalxB stops1 double mutant flies show the slow electroretinogram termination phenotype seen in stops1 single mutants.

The retinal degeneration seen in both CalxB and trp14 single mutant flies when they are maintained under a 12 hour light-12 hour dark cycle is suppressed in CalxB trp14 double mutants; most ommatidia in the double mutants contain the normal number of rhabdomeres at 14 days after eclosion.

The retinal degeneration seen in both CalxB and trp9 single mutant flies when they are maintained under a 12 hour light-12 hour dark cycle is suppressed in CalxB trp9 double mutants; most ommatidia in the double mutants contain the normal number of rhabdomeres at 14 days after eclosion.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Selected as: a homozygous viable mutation that disrupts the visual response.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (9)