FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Acsl1
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General Information
Symbol
Dmel\Acsl1
Species
D. melanogaster
Name
FlyBase ID
FBal0104593
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dAcsl1
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Amino acid numbering based on the 717aa isoform.

Amino acid replacement: V594D.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

T8681167A

Amino acid change:

V592D | Acsl-PA; V592D | Acsl-PB; V584D | Acsl-PC; V594D | Acsl-PD; V592D | Acsl-PE; V584D | Acsl-PF; V584D | Acsl-PG; V592D | Acsl-PH; V584D | Acsl-PI; V605D | Acsl-PJ

Reported amino acid change:

V594D

Comment:

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

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 )
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

About 12% of Acsl1/Df(2R)H3E1 mutant embryos display segmentation defects such as segment fusion or deletion. The segments A2-A7 are most frequently affected.

Among the Acsl1 maternal mutant embryos, approximately 11% show partial deletion or fusion of the abdominal segments. Removal of the zygotic contribution enhances the phenotypic percentage to 15%. The segments A1-A7 are most frequently affected.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

kni1/+ significantly increases the fraction of embryos showing segmentation defects caused by maternal mutant homozygous Acsl1. The segmentation abnormalities become more severe as indicated by more segments being disrupted in each mutant embryo.

Kr1/+ significantly enhances the percentage of segmentation-impaired embryos caused by maternal mutant homozygous Acsl1, although the severity is not obviously changed.

hb12/+ does not cause any detectable change in the segmentation phenotype of homozygous maternal mutant Acsl1 embryos.

Xenogenetic Interactions
Statement
Reference

Expression of Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC or Hsap\ACSL3Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4tub partially rescues the lethality associated with the Acsl8/Acsl1 genotype.

Expression of Hsap\ACSL4R570S.Scer\UAS.L.T:Hsap\MYC or Hsap\ACSL4P375L.Scer\UAS.L.T:Hsap\MYC under the control of Scer\GAL4tub fails to rescue the lethality associated with the Acsl8/Acsl1 genotype.

Complementation and Rescue Data
Partially rescued by
Comments

Expression of AcslScer\UAS.715.T:Hsap\MYC.C under the control of Scer\GAL4tub partially rescues the lethality associated with the Acsl8/Acsl1 genotype.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (6)