FlyBase Allele Report: Dmel\Calx[A]

General Information

Symbol

Dmel\Calx^A

Species

D. melanogaster

Name

FlyBase ID

FBal0193744

Feature type

allele

Associated gene

Dmel\Calx

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Wang et al., 2005)

Progenitor genotype

Cytology

Description

Amino acid replacement: T822I.

(Wang et al., 2005)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:21,012,414..21,012,414 [+]

Nucleotide change:

C21012414T

Amino acid change:

Reported amino acid change:

T822I

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Wang et al., 2005)

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

abnormal neurophysiology

(Wang et al., 2005)

abnormal neurophysiology, with Calx^ninaE.PW

(Wang et al., 2005)

abnormal neurophysiology (with Calx^ninaE.PW)

(Wang et al., 2005)

short lived

(Mok et al., 2020)

short lived (with Calx^B)

(Mok et al., 2020)

viable

(Wang et al., 2005)

Phenotype Manifest In

eye, with Calx^ninaE.PW

(Wang et al., 2005)

eye (with Calx^ninaE.PW)

(Wang et al., 2005)

eye photoreceptor cell

(Wang et al., 2005)

rhabdomere

(Wang et al., 2005)

Detailed Description

Statement

Reference

In Calx^A mutant flies, almost every aspect of phototransduction is defective. Upon termination of a blue light stimulus, electroretinograms from Calx^A flies show no prolonged depolarization afterpotential. Intracellular photoreceptor recordings and whole-cell ommatidial recordings from Calx^A flies show an inactivation phenotype in response to dark adaptation for 10 minutes followed by exposure to a 5s orange light pulse. Whole-cell recordings of the response of Calx^A isolated ommatidia to a 5s light pulse show a transient photoresponse of smaller amplitude than in wild-type, which decays more quickly to the baseline. Calx^A photoreceptors show a severe defect in subsequent dark adaptation and remain desensitized for 1 minute.

Pre-exposure to light for 0.5s has little impact on the slow termination of the photoresponse seen in electroretinograms of dark-adapted wild-type flies. In contrast, the electroretinograms of Calx^A flies exhibit hyperadaptation as the rate of photoresponse termination increases significantly after preexposing flies to light compared to dark adaption without preexposure.

The amplitude and integral currents (called quantum bumps) generated by a single photon of light is much smaller in Calx^A flies compared to wild-type flies. The small quantum bump amplitudes and waveforms produced by these mutants correlate with low Na/Ca currents. Furthermore, the Na⁺/Ca⁺ exchange current which can be induced in wild-type photoreceptor cells cannot be observed in Calx^A photoreceptors and resting Ca⁺ levels are elevated in Calx^A relative to wild-type photoreceptor cells.

Calx^A flies exposed to a 12 hour light/12 hour dark cycle undergo an age-dependent loss of the deep pseudopupil in the compound eye. Calx^A flies that are less than 2 days old have a deep pseudopupil, but by 8 days posteclosion the pseudopupil is eliminated. In contrast, Calx^A flies incubated in the dark do not lose the deep pseudopupil. A more detailed observation of this degeneration phenotype reveals that the eye of 7-day-old Calx^A light-reared flies contain few rhabdomeres although R7 cell rhabdomeres are observed in some ommatidia. However, all seven rhabdomeres are present in Calx^A flies that have been reared in the dark.

Calx^A flies that express Calx^ninaE.PW generate quantum bumps that are larger than wild-type and correlate with high Na/Ca currents.

(Wang et al., 2005)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT suppressed by

Statement

Reference

Calx^A has abnormal neurophysiology phenotype, non-suppressible by ninaC⁵

(Wang et al., 2005)

Phenotype Manifest In

NOT Suppressor of

Statement

Reference

Calx^A/Calx^A is a non-suppressor of retina | adult stage phenotype of Gαq^V303D

(Cao et al., 2018)

Calx^A/Calx^A is a non-suppressor of rhabdomere | adult stage phenotype of Gαq^V303D

(Cao et al., 2018)

Additional Comments

Genetic Interactions

Statement

Reference

The rapid light-dependent retinal degeneration characteristic observed in Gαq^V303D adult mutants is not rescued by combination with Calx^A.

(Cao et al., 2018)

The hyperadaptation phenotype seen in Calx^A single mutant flies is suppressed in inaC²; Calx^A double mutants as inaC²; Calx^A dark-adapted double mutant flies show a similar long termination rate in response to a flash of light as inaC² single mutants.

The hyerpadaptation phenotype of Calx^A dark-adapted flies is not suppressed in ninaC⁵; Calx^A double mutant flies.

(Wang et al., 2005)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Calx^E

(Wang et al., 2005)

Calx^D

(Wang et al., 2005)

Calx^C

(Wang et al., 2005)

Calx^B

(Wang et al., 2005)

Partially rescued by

Calx^A is partially rescued by Calx^1.hs.PW

(Wang et al., 2005)

Calx^A is partially rescued by Calx^2.hs.PW

(Wang et al., 2005)

Calx^A is partially rescued by Calx^ninaE.PW

(Wang et al., 2005)

Comments

Calx^A mutant flies that express either Calx^1.hs.PW or Calx^2.hs.PW show an essentially wild-type visual response. Normal morphology is restored to the eyes of Calx^1.hs.PW; Calx^A flies. However, the Na⁺/Ca⁺ exchange current that is missing in Calx^A photoreceptors can only be partially restored when these photoreceptors express Calx^1.hs.PW.

Expression of Calx^ninaE.PW in Calx^A photoreceptor cells rescues the ability of the Calx^A photoreceptors to produce a Na⁺/Ca⁺ exchange current; in fact, this exchange current is ~8-fold larger and ~5-fold faster than that produced by wild-type cells. Additionally, expression of Calx^ninaE.PW prevents the age-dependent loss of the depp pseudopupil from the eyes of Calx^A flies. Calx^ninaE.PW; Calx^A eyes have rhabdomeres 1-6, which are rarely present in Calx^A eyes (rhabdomere 7 is not rescued by Calx^ninaE.PW due to its expression pattern).

(Wang et al., 2005)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

24496

w^*; Calx^A

Notes on Origin

Discoverer

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

(Wang et al., 2005)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Calx^A

(Mok et al., 2020)

calx^A

(Liu et al., 2020, Cao et al., 2018, Elsaesser et al., 2010, Satoh et al., 2010, Wang et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (6)

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