FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Src42Amyri
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General Information
Symbol
Dmel\Src42Amyri
Species
D. melanogaster
Name
myristoylation
FlyBase ID
FBal0103954
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Src42Amiri
Key Links
Genomic Maps

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

Amino acid replacement: G2D.

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

G5982422A

Amino acid change:

G2D | Src42A-PA; G2D | Src42A-PC

Reported amino acid change:

G2D

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 ( 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

In Src42Amyri mutant embryos the extension of the dorsal branches lags behind the normally concurrent process of dorsal closure. The dorsal branches also contain fewer stalk cells. The dorsal trunk is a zigzag shape.

Src42Amyri embryos exhibit defects in leading edge cells: the actomyosin cable is disrupted and dorsal closure is slightly defective. 8% of stage 16 embryos show a very small dorsal hole and the remainder show an irregular arrangement of dorsal hairs. Embryonic lethality is 63% with 60% of unhatched embryos showing malformed mouthparts and a small anterior hole.

50.0 +/- 3.3% of homozygotes die as embryos and most of the remainder die during the first larval instar stage. Homozygous embryos do not show a dorsal open phenotype but have malformed mouth parts.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
Suppressor of
Phenotype Manifest In
Enhanced by
Statement
Reference

Src42Amyri has embryonic leading edge cell & actomyosin phenotype, enhanceable by Df(3L)FER-Δ1

Src42Amyri has embryonic leading edge cell & actomyosin phenotype, enhanceable by FERΔex1

Suppressed by
Other
Additional Comments
Genetic Interactions
Statement
Reference

Approximately 90% of Src42Amyri; p130CAS1 double mutants have holes in or completely absent head cuticles and 10% of these embryos exhibit germ band retraction cuticle defects.

Src64BPI enhances the tracheal defects seen in Src42Amyri mutant embryos. Many dorsal branches fail to extend correctly, remaining in a multicellular state despite the progression of dorsal closure.

Src42Amyri; Fps85DΔex1 double mutant embryos show an enhanced embryonic phenotype compared to Src42Amyri embryos. Src42Amyri; Fps85DΔex1 leading edge cells show a greater disruption of the actomyosin cable, resulting in a more irregular profile. The embryos show delayed dorsal closure, as 85% are still undergoing closure at late stage 16. Embryonic lethality is increased to 100% (vs 63% in Src42Amyri embryos). 95% of the double mutant embryos show breaks and irregularities in the dorsal hair pattern and a small anterior hole in the mouthparts. The remaining embryos fail to complete dorsal closure and have a large anterior hole.

Src42Amyri; Df(3L)Fps85D-Δ1 embryos show an enhancement of the embryonic phenotypes of both Src42Amyri and Df(3L)Fps85D-Δ1 single mutants. The leading edge cells of Src42Amyri; Df(3L)Fps85D-Δ1 embryos are highly irregular and show a complete loss of the F-actin cable. Cuticle preparations from these embryos show that 30% have a large anterior hole, 59% show a small anterior hole with small scabs along the dorsal midline and the remaining 11% fail to secrete a cuticle.

Btk29Ak00206 Src42Amyri/Btk29Ak05610 Src42Amyri double homozygotes show complete embryonic lethality and some embryos have a dorsal open phenotype. The leading edge cells are only partially elongated during dorsal closure. The dorsal open phenotype is partially rescued by JraAsp.hs.sev. Src42Amyri; Src64BPI double homozygous embryos have a mild but clear dorsal open phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
myristoylation
Secondary FlyBase IDs
    References (5)