FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Gyc76CKG03723ex173
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General Information
Symbol
Dmel\Gyc76CKG03723ex173
Species
D. melanogaster
Name
FlyBase ID
FBal0213072
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
gyc76CEx173
Key Links
Nature of the Allele
Cytology
Description

Imprecise excision of the P{SUPor-P} element, resulting in deletion of ~8kb of genomic sequence including a Gyc76C exon.

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

Gyc76CKG03723ex173/+ embryos exhibit an increase in embryonic ISNb motor axon defects as compared to controls.

Gyc76CKG03723ex173/+ and Gyc76CKG03723ex173/Gyc76CKG03723ex173 embryos show no apparent differences in muscle development or organization.

Gyc76CKG03723ex173/Gyc76CKG03723ex173 embryos exhibit abnormal motor axon pathways in both ISNb and SNa motor neurons.

Gyc76CKG03723ex173 homozygous and Gyc76CKG03723ex173/Gyc76C2388 heterozygous embryos display a severe salivary gland migration defect where mutant gland fail to turn completely and some glands appear branched or folded.

Patterning of the ventral and lateral somatic muscles is abnormal in homozygous and Gyc76CKG03723ex173/Gyc76C2388 embryos, whereas dorsal muscles are patterned normally.

Gyc76CKG03723ex173 embryos show motor axon guidance defects as ISNb and SNa axons often fail to defasciculate and do not innervate their proper muscle targets. Gyc76CKG03723ex33/Gyc76CKG03723ex173 and Gyc76CKG03723ex173/Df(3L)5126 embryos show the same phenotype. Gyc76CKG03723/+ heterozygotes show a milder version of this phenotype.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference

Gyc76CKG03723ex173 has abnormal neuroanatomy | dominant phenotype, non-enhanceable by ena[+]/enaGC10

NOT suppressed by
Statement
Reference

Gyc76CKG03723ex173 has abnormal neuroanatomy | dominant phenotype, non-suppressible by ena[+]/enaGC10

Enhancer of
Statement
Reference
NOT Enhancer of
Suppressor of
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

kermitex31/+, Gyc76CKG03723ex173/+ double mutants exhibit an increased number of defects in both ISNb and SNa motor neuron axon pathways as compared to kermitex31/+ mutant embryos.

kermitex31/kermitex31, Gyc76CKG03723ex173/Gyc76CKG03723ex173 double mutant embryos exhibit a similar number of defects in ISNb motor neuron pathways as compared to kermitex31/kermitex31 or Gyc76CKG03723ex173/Gyc76CKG03723ex173 single mutant embryos, and a similar number of defects in SNa motor neuron pathways as compared to kermitex31/kermitex31 single mutant embryos.

The ISNb axon pathfinding, positioning and bypass defects caused by expression of Sema-1aScer\UAS.cYa under the control of Scer\GAL4Mef2.PR are significantly reduced in Gyc76CKG03723ex173/+ embryos.

Sema-1ak13702/+; Gyc76CKG03723ex173/+ double mutant embryos show a motor axon guidance phenotype that is similar in severity to Gyc76CKG03723ex173 homozygotes, while Gyc76CKG03723ex173 heterozygotes show a much milder phenotype. One copy of either Df(4)C3 or Df(3R)swp2MICAL also enhances the axon guidance phenotype of Gyc76CKG03723ex173/+ embryos.

The Gyc76CKG03723ex173/+ phenotype is not modified in enaGC10/+; Gyc76CKG03723ex173/+ double mutants.

A Gyc76CKG03723ex173 background partially suppresses the aberrant axon midline-crossing phenotype of embryos that express plexAScer\UAS.cWa under the control of Scer\GAL4elav.PLu.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Gyc76CScer\UAS.FL.T:Hsap\MYC under the control of Scer\GAL4elav.PU partially rescues the ISNb and SNa motor neuron axon pathway phenotypes of Gyc76CKG03723ex173/Gyc76CKG03723ex173 embryos.

Expression of Gyc76CΔEcto.Scer\UAS.T:Hsap\MYC, Gyc76CΔKHD.Scer\UAS.T:Hsap\MYC, Gyc76CΔDD.Scer\UAS.T:Hsap\MYC, Gyc76CΔCterm.Scer\UAS.T:Hsap\MYC, Gyc76CΔEndo.Scer\UAS.T:Hsap\MYC, or Gyc76CΔPBM.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4elav.PU fails to rescue the ISNb and SNa motor neuron axon pathway phenotypes of Gyc76CKG03723ex173/Gyc76CKG03723ex173 embryos.

Expression of Gyc76CScer\UAS.T:Hsap\MYC in either the salivary glands or mesoderm, under the control of Scer\GAL4fkh.PH or Scer\GAL4twi.PB significantly rescues the gland migration defect found in Gyc76C2388 homozygous embryos. Simultaneous expression of Gyc76CScer\UAS.T:Hsap\MYC in the salivary gland and mesoderm does not result in increased rescue of the migration defect compared to expression in either tissue alone.

Expression of Gyc76CScer\UAS.T:Hsap\MYC in all neurons under the control of Scer\GAL4elav.PLu significantly, but not completely, rescues the motor axon guidance and lethality phenotypes of Gyc76CKG03723ex173 embryos.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Symbol Synonym
Gyc76CKG03723ex173
gyc76CEx173
gyc76CKG03723ex173
Name Synonyms
Secondary FlyBase IDs
    References (4)