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General Information
Symbol
Dmel\Acsl8
Species
D. melanogaster
Name
FlyBase ID
FBal0155128
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dAcsl8
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

G8681505A

Amino acid change:

W683term | Acsl-PA; W683term | Acsl-PB; W675term | Acsl-PC; W685term | Acsl-PD; W683term | Acsl-PE; W675term | Acsl-PF; W675term | Acsl-PG; W683term | Acsl-PH; W675term | Acsl-PI; W696term | Acsl-PJ

Reported amino acid change:

W685term

Comment:

G to A nucleotide change at the second or third position of the Trp codon leads to a nonsense mutation (exact site of mutation unspecified). Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Nucleotide change:

A8680080G

Amino acid change:

K292E | Acsl-PA; K292E | Acsl-PB; K284E | Acsl-PC; K294E | Acsl-PD; K292E | Acsl-PE; K284E | Acsl-PF; K284E | Acsl-PG; K292E | Acsl-PH; K284E | Acsl-PI; K305E | Acsl-PJ

Reported amino acid change:

K294E

Comment:

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

Nucleotide change:

A8680456G

Amino acid change:

Q417R | Acsl-PA; Q417R | Acsl-PB; Q409R | Acsl-PC; Q419R | Acsl-PD; Q417R | Acsl-PE; Q409R | Acsl-PF; Q409R | Acsl-PG; Q417R | Acsl-PH; Q409R | Acsl-PI; Q430R | Acsl-PJ

Reported amino acid change:

Q419R

Comment:

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

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid numbering based on the 717aa isoform.

This mutation effectively removes the last 33 amino acids.

Amino acid replacement: K294E.

Amino acid replacement: Q419R.

Amino acid replacement: W685term.

Amino acid replacement: ??term.

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

Neuromuscular junction 4 (NMJ4) terminals look similar across larval abdominal segments A3-A6 in wild type. However, in Acsl05847/Acsl8 mutants, NMJs innervating the anterior segment muscles have shorter axons that are overgrown with more satellite boutons, whereas those innervating the posterior segment muscles have longer axons and are dystrophic with relatively few boutons.

About 18% of Acsl8/Df(2R)H3E1 mutant embryos display segmentation defects.

Among the Acsl8 maternal mutant embryos, approximately 59% show segmentation defects. The segments A1-A7 are most frequently affected.

Neutral lipid accumulation is blocked in Acsl8/Acsl05847 wing discs.

Total triacylglycerol content of Acsl8/Acsl05847 pharates is significantly lower than wild type.

The normally defined pattern of axon projection in the optic lamina of the third instar larval brain is disrupted in the Acsl8/Acslk10313 mutant.

The following phenotypes are observed in the optic ganglia of Acsl8/Acslk10313 mutants: lamina neurons are significantly reduced in number, the normally fine alignment of glial cells disappears, the lamina plexus is in disarray, the number of glial cells in the medulla is greatly decreased, axon termination in the medulla is barely observed.

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

Acsl05847/Acsl8 has neuromuscular junction phenotype, enhanceable by Dadj1E4/Dad[+]

Acsl05847/Acsl8 has NMJ bouton | increased number phenotype, enhanceable by Dadj1E4/Dad[+]

Acsl05847/Acsl8 has neuromuscular junction phenotype, enhanceable by Rab1193Bi/Rab11[+]

Suppressed by
NOT suppressed by
Additional Comments
Genetic Interactions
Statement
Reference

Dadj1E4/+ significantly increases synaptic overgrowth of Acsl05847/Acsl8 mutants.

Rab1193Bi/+ and, to a greater extent, Rab1193Bi/Rab1193Bi significantly increases neuromuscular junction overgrowth of Acsl05847/Acsl8 mutants.

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 and Acsl8/Acsl05847 genotypes.

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 and Acsl8/Acsl05847 genotypes.

Expression of Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC, Hsap\ACSL4Scer\UAS.S.T:Hsap\MYC or Hsap\ACSL3Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4tub restores neutral lipid staining in Acsl8/Acsl05847 wing discs.

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 restore neutral lipid staining in Acsl8/Acsl05847 wing discs.

Expression of Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC under the control of Scer\GAL4tub restores normal triacylglycerol levels in Acsl8/Acsl05847 wing discs.

Expression of Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC under the control of Scer\GAL4tub restores well-ordered axon projection in the optic lamina of the third instar larval brain of Acsl8/Acslk10313 mutants.

Expression of Hsap\ACSL4P375L.Scer\UAS.L.T:Hsap\MYC or Hsap\ACSL4R570S.Scer\UAS.L.T:Hsap\MYC under the control of Scer\GAL4tub fails to restore well-ordered axon projection in the optic lamina of the third instar larval brain of Acsl8/Acslk10313 mutants.

Complementation and Rescue Data
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 and Acsl8/Acsl05847 genotypes.

Expression of AcslScer\UAS.715.T:Hsap\MYC.C under the control of Scer\GAL4tub restores neutral lipid staining in Acsl8/Acsl05847 wing discs.

Expression of AcslScer\UAS.715.T:Hsap\MYC.C under the control of Scer\GAL4tub restores well-ordered axon projection in the optic lamina of the third instar larval brain of Acsl8/Acslk10313 mutants.

Expression of AcslScer\UAS.715.T:Hsap\MYC.C under the control of Scer\GAL4dpp.blk1 fails to restore well-ordered axon projection in the optic lamina of the third instar larval brain of Acsl8/Acslk10313 mutants.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Comparing Acsl8, Acsl1, Acslk10313 and Acsl05847, Acsl8 is the strongest mutation based on its lethal stage.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (6)