FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Ace1
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General Information
Symbol
Dmel\Ace1
Species
D. melanogaster
Name
FlyBase ID
FBal0000182
Feature type
allele
Associated gene
Dmel\Ace
Associated Insertion(s)
Carried in Construct
Also Known As
Acel26, l(3)26
Key Links
Genomic Maps

Allele class

hypomorphic allele - genetic evidence

loss of function allele

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Incardona and Rosenberry, 1996)

loss of function allele

(Zador, 1995)
Mutagen
X ray
(Fournier et al., 1989, Nagoshi and Gelbart, 1987, Hilliker et al., 1981)
Progenitor genotype
Cytology

Polytene chromosomes normal.

(Nagoshi and Gelbart, 1987)
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
insertion
3R:13,239,973..13,242,998 [-]
Linked to:
HindIII-HindIII restriction fragment
Comment:

5kb of unknown DNA inserted within a HindIII fragment within the fifth intron; position of restriction fragment on reference sequence inferred by FlyBase curator

(Fournier et al., 1989, Nagoshi and Gelbart, 1987)
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

      Lethal phase is late embryonic/early larval.

      (Hall and Kankel, 1976)

      Lethality at end of embryonic stage. AChE-minus tissues survive in mosaics unless enzyme absent from posterior midbrain; surviving mosaics have defective visual physiology, optomotor behavior, or courtship depending on location of mutant clone. Such clones associated with defective morphology of neuropil of various ganglia in central nervous system.

      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      Acelm38/Ace1 is rescued by Ace+mFa

      (Incardona and Rosenberry, 1996)
      Partially rescued by

      Acelm38/Ace1 is partially rescued by AceTM.Tag:TM(HSV1-gC)

      (Incardona and Rosenberry, 1996)
      Comments

      Acelm38/Ace1 flies rescued by Ace+mFa occasionally show a bang-sensitive phenotype; flies subjected to mechanical shock sometimes produce a burst of uncoordinated motor activity followed by paralysis, from which they recover in approximately 30 seconds. Ace1/Acelm38 flies carrying two copies of AceTM.T:Hsim\gC are viable, although adults are often bang-sensitive.

      (Incardona and Rosenberry, 1996)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer

      Schalet, Kernaghan and Chovnick, 1964.

      (Hall and Kankel, 1976)

      Induced with: ry26.

      FlyBase curator comment: FBrf0050439 states that Ace1 is caused by the insertion of unknown DNA into the fifth intron at coordinate +30, however, FBrf0046381 shows that this insertion of DNA is separable from the Ace1 mutation by recombination.

      (Fournier et al., 1989)

      The Ace1 chromosome contains an insertion of approximately 5kb that is not present in Canton-S or Oregon-R flies. The parental chromosome for Ace1 was never isolated and recombination analysis shows that the 5kb insertion is separable from the Ace1 mutation by recombination.

      (Nagoshi and Gelbart, 1987)
      Comments
      Comments

      Greatly reduced levels of acetylcholinesterase.

      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (7)
      References (14)