FB2026_02 , released June 18, 2026
Allele: Dmel\Ctr1A25
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General Information
Symbol
Dmel\Ctr1A25
Species
D. melanogaster
Name
FlyBase ID
FBal0240787
Feature type
allele
Associated gene
Dmel\Ctr1A
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Turski and Thiele, 2007)
Mutagen
P-element activity
(Turski and Thiele, 2007)
Progenitor genotype
Ctr1AG788
(Turski and Thiele, 2007)
Cytology
Description

A 5,148-bp deletion that removes most of the coding sequence of Ctr1A, but leaves the upstream gene, CG3224, intact.

(Turski and Thiele, 2007)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
deletion
X:6,661,736..6,666,883 [+]
Comment:

Approximate boundaries of a 1,148bp deletion resulting from the imprecise excision of P{EP}Ctr1AG788 that removes most of the Ctr1A coding sequence. It is not clear from Fig. 2 if the deletion includes any sequences upstream from the insertion.

(Turski and Thiele, 2007)
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Heterozygous Ctr1A25 mutant flies appear to have normal cardiac function as fractional shortening (FS) is comparable to controls.

      (Casad et al., 2012)

      Ctr1A25 mutants arrest in early larval stages and are deficient in the activity of copper-dependent enzymes. Raising the mutants on food containing different concentrations of copper (even when the parents are also kept on food supplemented with copper), fails to affect the Ctr1A25 phenotype.

      (Hua et al., 2010)

      First and second instar hemizygous Ctr1A25 mutant larvae demonstrate significant pigmentation defects of the mouth hook structures and spiracles. The pigmentation defects are more severe in mutant embryos and larvae lacking both maternal and zygotic Ctr1A.

      Ctr1A25 is essential for development, because hemizygous Ctr1A25 zygotic mutant larvae arrest as either 1st instar larvae (~40%) or as 2nd instar larvae ~60%). Ctr1A25 mutants lacking both maternal and zygotic Ctr1A arrest at earlier developmental stages than zygotic mutants. Approximately 40% of Ctr1A25 maternal and zygotic mutants arrest during embryogenesis, as compared with ~5% of zygotic mutants arresting at the embryonic stage. Ctr1A25 mutant larvae lacking both maternal and zygotic Ctr1A arrest earlier than the zygotic mutant larvae. However, a fraction of Ctr1A25 hemizygous zygotic mutants do survive to adulthood on food supplemented with extra copper ions. In contrast to copper, dietary zinc or iron supplements do not rescue Ctr1A25 mutants.

      Ctr1A25 escaper males exhibit hypo-pigmented abdomen and thoracic bristles.

      Ctr1A25 mutants are copper deficient. Heterozygous and hemizygous Ctr1A25 mutant larvae show approximately 20% and 30% reduction in copper levels, respectively.

      Ctr1A25 mutant 1st instar larvae lacking both maternal and zygotic Ctr1A exhibit lower heart beat rates than wild-type controls. Dietary copper supplementation significantly elevates the heart rate of Ctr1A25 maternal and zygotic mutant 1st instar larvae.

      (Turski and Thiele, 2007)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Overexpression of Ctr1BScer\UAS.cSa under the control of Scer\GAL4tub fails to suppress the lethality associated with developmental arrest found in Ctr1A25 mutants. This failure could be associated with toxicity caused by excessive copper uptake.

      Overexpression of Ctr1BScer\UAS.P\T.cHa under the control of Scer\GAL4tub suppresses the lethality associated with developmental arrest found in Ctr1A25 mutants.

      (Hua et al., 2010)

      Expression of Ctr1CScer\UAS.cSa under the control of Scer\GAL4tub.PU can fully suppress the lethality found in Ctr1A25 mutants.

      (Steiger et al., 2010)
      Xenogenetic Interactions
      Statement
      Reference

      Overexpression of Hsap\CTR1Scer\UAS.cHa under the control of Scer\GAL4tub.PU suppresses the lethality associated with developmental arrest found in Ctr1A25 mutants.

      (Hua et al., 2010)
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      Ctr1A25
      (Casad et al., 2012, Hua et al., 2010, Steiger et al., 2010)
      ctr1A25
      (Turski and Thiele, 2007)
      Name Synonyms
      Excision line 25
      (Turski and Thiele, 2007)
      Secondary FlyBase IDs
        References (4)