FlyBase Allele Report: Dmel\inaC[2]

General Information

Symbol

Dmel\inaC²

Species

D. melanogaster

Name

FlyBase ID

FBal0005600

Feature type

allele

Associated gene

Dmel\inaC

Associated Insertion(s)

Carried in Construct

Also Known As

inaC^P209, inaC²⁰⁹

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Hofstee and Stavenga, 1996, Hardie et al., 1993)

Mutagen

ethyl methanesulfonate

Progenitor genotype

Cytology

Description

Premature termination of the coding region.

(Matsumoto et al., 1994)

Amino acid replacement: W93term.

(Smith et al., 1991)

Nucleotide substitution: G279A.

(Smith et al., 1991)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:16,899,084..16,899,084 [+]

Nucleotide change:

G16899084A

Amino acid change:

W93term | inaC-PA

Reported amino acid change:

W93term

Comment:

Nonsense mutation (TGG to TGA) at Trp codon.

(Smith et al., 1991)

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

(Popescu et al., 2006, Rajaram et al., 2005, Wang et al., 2005, Adamski et al., 1998, Hardie et al., 1993)

abnormal neurophysiology | recessive

(Wang et al., 2008)

abnormal neurophysiology | semidominant

(Wang et al., 2008)

abnormal visual behavior

(Gu et al., 2005)

abnormal visual behavior | recessive

(Hardie et al., 1993)

Phenotype Manifest In

eye

(Wang et al., 2005)

photoreceptor

(Gu et al., 2005)

photoreceptor neuron

(Hofstee and Stavenga, 1996, Ranganathan et al., 1991, Smith et al., 1991)

retina

(Popescu et al., 2006)

Detailed Description

Statement

Reference

All the photoreceptor cells are still present in 21 day old inaC²/+ flies.

(Venkatachalam et al., 2010)

inaC² heterozygotes display ERG (electroretinogram) with slow deactivation kinetics, and homozygotes exhibit more severe deactivation defects, when stimulated with 5s of bright light. Only homozygotes display response inactivation as the receptor potential rapidly declines during the light pulse. The half-deactivation time for inaC² heterozygotes is about twice that of controls and one third that of homozygotes. Both the homozygous and heterozygous inaC² mutants show defects in light adaptation.

(Wang et al., 2008)

In inaC² mutants, individual photoreceptors form the correct number of synapses per

presynaptic terminal independently of cartridge composition.

(Hiesinger et al., 2006)

In red-eyed inaC² homozygous flies flies dark-adapted for 2 minutes, the electro-retinogram (ERG) response to 2 second white-light stimulation displays the initial fast depolarization seen in wild-type but, unlike wild-type, depolarisation is not maintained during stimulation and the membrane potential returns gradually to baseline following depolarisation. This phenotype is seen at both low and high light levels.

(Popescu et al., 2006)

Responses to brief flashes (~100 photons) during substitution with 40 mM Na⁺ in inaC² mutants are initially indistinguishable from those in the wild type but fail to terminate normally, leaving a long tail, which decays over a period of ~1 second. As Ca²⁺ is raised, both the peak response and the tail of the response are indistinguishable from parallel experiments on wild-type flies.

(Gu et al., 2005)

inaC² mutants display retinal axon termination responses that are comparably slow after both long (3-seconds) and short (0.2-seconds), compared to wild-type.

(Rajaram et al., 2005)

inaC² dark-adapted mutant flies show a longer termination rate in response to a 0.5s flash of light compared to wild-type flies.

(Wang et al., 2005)

Linolenic acid can activate light sensitive channels in mutant photoreceptors.

(Chyb et al., 1999)

inaC² flies raised under 12 hour light:dark conditions retain a deep pseudopupil for at least 15 days.

(Paetkau et al., 1999)

Homozygotes have an abnormal electroretinogram (ERG) characterised by a slowly decaying receptor potential during the light pulse and delayed deactivation upon cessation of light stimulation. inaC² inaD¹ double mutants show abnormal ERGs with response inactivation; they show a marked reduction in response to a second pulse of light.

(Adamski et al., 1998)

Mutants exhibit long latencies and reduced initial slopes: activation of the visual response is delayed. Following termination of light repolarisation is prolonged. The deactivation waveform of norpA^C1094S.hs inaC² double mutants is similarly delayed as in norpA^C1094S.hs but requires more time to completely repolarise and the latency to activation is almost identical to that of norpA^C1094S.hs.

(Shieh et al., 1997)

The initial reflectance is distinctly higher than that of wild type, demonstrating the pigment granules are not fully withdrawn from the rhabdomere. The light sensitivity of the pigment migration is slightly raised compared to wild type. The peak of the pulse response is reached distinctly later than that in wild type, suggesting a defect in the deactivation mechanism of inaC.

(Hofstee and Stavenga, 1996)

Does not abolish Ca²⁺-dependent inactivation of light-sensitive channels in photoreceptors. Shows rapid inactivation of transient currents induced by hyperpolarization in photoreceptors.

(Hardie and Minke, 1994)

Shows an increased light-induced decrease in extracellular Ca²⁺ concentration compared to the wild-type. This increase is blocked by trp¹.

(Peretz et al., 1994)

Light adaptation severely reduced. Inactivation and response compression may reflect exhaustion of the excitatory process.

(Hardie et al., 1993)

Photoreceptors of homozygotes are unable to carry out normal rapid deactivation after a light stimulus, due to a defect in the calcium-dependent deactivation mechanism. Excitation mechanisms appear to be unaffected.

(Ranganathan et al., 1991)

Mutant photoreceptors are abnormal in response to light; deactivation kinetics and rapid desensitisation are defective. Mutant photoreceptors show significant hyperadaptation to light relative to wild-type cells.

(Smith et al., 1991)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

inaC² has abnormal neurophysiology | semidominant phenotype, suppressible by mts^XE-2258/mts[+]

(Wang et al., 2008)

NOT suppressed by

Statement

Reference

inaC² has abnormal neurophysiology | semidominant phenotype, non-suppressible by mts^XE-2258/mts[+]

(Wang et al., 2008)

inaC² has abnormal neurophysiology | recessive phenotype, non-suppressible by mts^XE-2258/mts[+]

(Wang et al., 2008)

Phenotype Manifest In

Suppressor of

Statement

Reference

inaC² is a suppressor of photoreceptor cell R4 phenotype of rdgB⁵

(Smith et al., 1991)

inaC² is a suppressor of photoreceptor cell R5 phenotype of rdgB⁵

(Smith et al., 1991)

inaC² is a suppressor of photoreceptor cell R6 phenotype of rdgB⁵

(Smith et al., 1991)

inaC² is a suppressor of photoreceptor cell R1 phenotype of rdgB⁵

(Smith et al., 1991)

inaC² is a suppressor of photoreceptor cell R2 phenotype of rdgB⁵

(Smith et al., 1991)

inaC² is a suppressor of photoreceptor cell R3 phenotype of rdgB⁵

(Smith et al., 1991)

NOT Suppressor of

Statement

Reference

inaC² is a non-suppressor of eye photoreceptor cell phenotype of rdgB⁹

(Paetkau et al., 1999)

inaC² is a non-suppressor of ommatidium phenotype of rdgB⁹

(Paetkau et al., 1999)

inaC² is a non-suppressor of eye photoreceptor cell phenotype of rdgB^ota1

(Paetkau et al., 1999)

inaC² is a non-suppressor of ommatidium phenotype of rdgB^ota1

(Paetkau et al., 1999)

Other

Statement

Reference

Hsap\KCNJ2^{R228Q.UAS.EGFP}, inaC² has photoreceptor phenotype

(Gu et al., 2005)

Additional Comments

Genetic Interactions

Statement

Reference

The deactivation defect seen in inaC² heterozygotes is rescued in a mts^XE-2258 heterozygous background. Contrarily, heterozygosity of mts^XE-2258 fails to rescue the inactivation defect of inaC² homozygotes. inaC² heterozygotes and homozygotes display a deficiency in light adaptation, which fails to be rescued in both genotypes when in combination with mts^XE-2258/+.

(Wang et al., 2008)

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.

(Wang et al., 2005)

inaC² does not significantly alter the deep pseudopupil loss of rdgB^ota1 or rdgB⁹ flies and fails to suppress the photoreceptor degeneration and ommatidial disorganisation seen in these flies at 6 days after eclosion.

(Paetkau et al., 1999)

Suppresses the light-dependent photoreceptor degeneration phenotype of rdgB⁵ flies.

(Smith et al., 1991)

Xenogenetic Interactions

Statement

Reference

In inaC² photoreceptors expressing Hsap\KCNJ2^{R228Q.Scer\UAS.T:Avic\GFP-EGFP} channels, the PIP₂-sensitive current is suppressed by more than 50%, while it is only suppressed by 20% in wild-type photoreceptors. After depletion, the Hsap\KCNJ2^{R228Q.Scer\UAS.T:Avic\GFP-EGFP} current recovers in the dark as PIP₂ is resynthesised with a timecourse that is indistinguishable from controls.

(Gu et al., 2005)

Complementation and Rescue Data

Rescued by

inaC² is rescued by inaC^hs.PA

(Adamski et al., 1998)

inaC² is rescued by inaC^+tSa

(Smith et al., 1991)

Not rescued by

inaC² is not rescued by inaC^I700D.hs

(Adamski et al., 1998)

Comments

The photoreceptor phenotype is completely rescued by inaC^+tSa.

(Smith et al., 1991)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

42241

w^*; inaC²

Notes on Origin

Discoverer

Pak.

Comments

Retinal homogenate is capable of phosphorylating endogenous Arr2 in vitro.

(Matsumoto et al., 1994)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

P209

inaC²⁰⁹

(Mishra et al., 2007, Iakhine et al., 2001, Tsunoda et al., 2001, Paetkau et al., 1999, Hardie and Minke, 1994, Ranganathan et al., 1991, Smith et al., 1991)

inaC²

(Meyer et al., 2008)

inaC^p209

(Hiesinger et al., 2006, Popescu et al., 2006, Adamski et al., 1998, Shieh et al., 1997)

Name Synonyms

Secondary FlyBase IDs

References (33)

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