FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Wnt4EMS23
Open Close
General Information
Symbol
Dmel\Wnt4EMS23
Species
D. melanogaster
Name
FlyBase ID
FBal0141320
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DWnt4EMS23
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: ?343term.

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

G7256874A

Amino acid change:

W346term | Wnt4-PA; W346term | Wnt4-PB

Reported amino acid change:

?343term

Comment:

Approximate location of nonsense mutation in Wnt4EMS23. Curator note: The mapped location is 3 aa downstream of the reported location because the codon at position 346 is GAC, which requires two nucleotide changes to create a nonsense mutation and the reported location of Wnt4C1 from the same paper appears to be 3aa upstream of its location in the reference sequence.

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 ( 1 )
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

Homozygous Wnt4EMS23 and transheterozygous Wnt4EMS23/Df(2L)BSC226 embryos have cardioblast alignment defects obvious at stage 14, worsening as development progresses and resulting in gaps within the heart tube. In contrast, cardiac progenitor cell specification and pericardial cells are not affected.

In Wnt4EMS23 homozygous embryos, ostia cell progenitors fail to undergo the cellular constriction typically observed in wild-type hearts. This impairs ostia cell formation and leads to loss of ostia.

One copy of Wnt4EMS23 has no effect on hemocyte proliferation in third instar larvae.

Mutant embryos have salivary gland guidance defects; the entire salivary gland is curved ventromedially, instead of lying parallel to the midline as in wild-type embryos. This defect is seen as early as stage 12.

Wnt4C1/Wnt4EMS23 mutant exhibit occasional misrouting of ventral axons towards the dorsal lamina. In extreme cases, ventral axons appear as if they are about to project to ventral lamina but then veer towards the dorsal lamina. Ventral misrouting is seen in the larval optic stalk.

Dorsal cluster neuron axon extension is not affected in Wnt4EMS23/+ flies.

Lethality acts in first or second larval instar. 10%-15% of mutants survive to adulthood. Survivors are sterile, though show no external defects. Phenotype of homozygotes is similar to that of hemizygotes.

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

Wnt4[+]/Wnt4EMS23 is a suppressor of visible | adult stage phenotype of Nab2EP3716, Scer\GAL4GMR.PU

Phenotype Manifest In
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Wnt4[+]/Wnt4EMS23 is a suppressor of eye phenotype of Nab2EP3716, Scer\GAL4GMR.PU

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Wnt4EMS23/Wnt4P23 does not enhance the neuronal targeting defect seen in Df(3R)Tl-X/Df(3R)ro-XB3 embryos, in which the nerve terminals synapsed to muscle M12 are greatly reduced and the nerve terminals synapsed to muscle M13 are expanded compared to controls.

Wnt5D7 ; Wnt4EMS23 double mutants have a higher penetrance of salivary gland curving than is seen in either of the single mutants alone.

A hepr75 bacgkground enhances the Wnt4EMS23/+ R axon misrouting phenotype.

A Wnt4EMS23/+ background enhances the hepr75 R axon misrouting phenotype.

The addition of Wnt4EMS23 has no effect on the interneuron phenotype seen in drlScer\UAS.cCa, Scer\GAL4eg-Mz360 animals.

Xenogenetic Interactions
Statement
Reference

One copy of Wnt4EMS23 strongly enhances the hemocyte overproliferation seen in third instar larvae when Hsap\RUNX1::Hsap\RUNX1T1Scer\UAS.cSa is expressed under the control of Scer\GAL4Hml.Δ.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (19)