FlyBase Allele Report: Dmel\ATPsynδ[KK108804]

General Information

Symbol

Dmel\ATPsynδ^KK108804

Species

D. melanogaster

Name

FlyBase ID

FBal0235834

Feature type

allele

Associated gene

Dmel\ATPsynδ

Associated Insertion(s)

Carried in Construct

P{KK108804}

Key Links

Genomic Maps

JBrowse

Transgenic product class

RNAi_reagent

(Keleman et al., 2009.8.5)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

RNAi_reagent

(Keleman et al., 2009.8.5)

Mutagen

in vitro construct

(Keleman et al., 2009.8.5)

Progenitor genotype

Carried in construct

P{KK108804}

Cytology

Description

UASt regulatory sequences drive expression of an inverted repeat.

(Keleman et al., 2009.8.5)

Allele components

Component

Use(s)

Regulatory region(s)

UASt

binary expression system - regulatory region

Encoded product / tool

dsRNA-KK108804

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 1 )

Disease

Evidence

References

model of mitochondrial complex V (ATP synthase) deficiency nuclear type 5

CEC

(Oláhová et al., 2018)

CEC with Hsap\ATP5F1D^{P82L.UAS.Tag:V5}

(Oláhová et al., 2018)

CEC with Hsap\ATP5F1D^{V106G.UAS.Tag:V5}

(Oláhová et al., 2018)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of mitochondrial complex V (ATP synthase) deficiency nuclear type 5

is ameliorated by Hsap\ATP5F1D^{WT.UAS.Tag:V5}

(Oláhová et al., 2018)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

lethal, with Scer\GAL4^Act.PU

(Oláhová et al., 2018)

lethal, with Scer\GAL4^da.PU

(Oláhová et al., 2018)

lethal, with Scer\GAL4^elav-C155

(Oláhová et al., 2018)

lethal, with Scer\GAL4^Tub.PU

(Oláhová et al., 2018)

lethal - all die before end of pupal stage, with Scer\GAL4^ey.PU

(Oláhová et al., 2018)

visible | adult stage, with Scer\GAL4^ey.PU

(Oláhová et al., 2018)

Phenotype Manifest In

head, with Scer\GAL4^ey.PU

(Oláhová et al., 2018)

Detailed Description

Statement

Reference

The expression of ATPsynδ^KK108804 under the control of Scer\GAL4^ey.PU is almost pupal lethal.

(Oláhová et al., 2018)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

ATPsynδ^KK108804, Scer\GAL4^ey.PU has lethal - all die before end of pupal stage phenotype, suppressible by Hsap\ATP5F1D^{WT.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^ey.PU has lethal - all die before end of pupal stage phenotype, suppressible by Hsap\ATP5F1D^{P82L.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^ey.PU has lethal - all die before end of pupal stage phenotype, suppressible by Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^ey.PU has visible | adult stage phenotype, suppressible by Hsap\ATP5F1D^{WT.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^ey.PU has visible | adult stage phenotype, suppressible | partially by Hsap\ATP5F1D^{P82L.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^ey.PU has visible | adult stage phenotype, suppressible | partially by Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, Scer\GAL4^ey.PU

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^elav-C155 has lethal - all die before end of pupal stage phenotype, suppressible by Hsap\ATP5F1D^{WT.UAS.Tag:V5}, Scer\GAL4^elav-C155

(Oláhová et al., 2018)

NOT suppressed by

Statement

Reference

ATPsynδ^KK108804, Scer\GAL4^elav-C155 has lethal - all die before end of pupal stage phenotype, non-suppressible by Hsap\ATP5F1D^{P82L.UAS.Tag:V5}, Scer\GAL4^elav-C155

(Oláhová et al., 2018)

ATPsynδ^KK108804, Scer\GAL4^elav-C155 has lethal - all die before end of pupal stage phenotype, non-suppressible by Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, Scer\GAL4^elav-C155

(Oláhová et al., 2018)

Other

Statement

Reference

Phenotype Manifest In

Other

Statement

Reference

ATPsynδ^KK108804, Hsap\ATP5F1D^{P82L.UAS.Tag:V5}, Scer\GAL4^ey.PU has eye phenotype

(Oláhová et al., 2018)

ATPsynδ^KK108804, Hsap\ATP5F1D^{P82L.UAS.Tag:V5}, Scer\GAL4^ey.PU has antenna phenotype

(Oláhová et al., 2018)

ATPsynδ^KK108804, Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, Scer\GAL4^ey.PU has eye phenotype

(Oláhová et al., 2018)

ATPsynδ^KK108804, Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, Scer\GAL4^ey.PU has antenna phenotype

(Oláhová et al., 2018)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

The Scer\GAL4^ey.PU-driven expression of ATPsynδ^KK108804 in combination with either Hsap\ATP5F1D^{P82L.UAS.Tag:V5} or Hsap\ATP5F1D^{V106G.UAS.Tag:V5}, but not with Hsap\ATP5F1D^{WT.UAS.Tag:V5} leads to eye and antenna defects, including small, bar and glossy eye phenotypes.

The Scer\GAL4^ey.PU-driven expression of ATPsynδ^KK108804 in combination with Hsap\ATP5F1D^{WT.UAS.Tag:V5} leads to apparently normal electroretinograms, whereas the expression of ATPsynδ^KK108804 in combination with either Hsap\ATP5F1D^{P82L.UAS.Tag:V5} or Hsap\ATP5F1D^{V106G.UAS.Tag:V5} leads to severe decreases in amplitude, on-transients and off-transients.

(Oláhová et al., 2018)

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

VDRC

v100621

P{KK108804}VIE-260B

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

ATPsyn{delta}^RNAi

(Bonnay et al., 2020)

ATPsynδ^KK108804

l(1)G0230^KK108804

Name Synonyms

Secondary FlyBase IDs

References (3)

Report Sections

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