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General Information
Symbol
Dmel\fz2UAS.N
Species
D. melanogaster
Name
FlyBase ID
FBal0092982
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-DFz2N, UAS-DFz2-DN
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference
Coding sequence downstream of nucleotide 174 (FBrf0089594) replaced with coding sequence nucleotides 174-1030, plus sequence RWL-stop. The result is a fusion of extracellular and first transmembrane domains with an intracellular DTRWL at the carboxy-terminus, analogous to fzUAS.N.
Allele components
Product class / Tool use(s)
Encoded product / tool
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
The expression of fz2Scer\UAS.N under the control of Scer\GAL4Mhc.PW leads to the dorsal longitudinal indirect flight muscles exhibiting mitochondria defects, including abnormal morphology, sparse and collapsed cristae, and a significant decrease in electron density in electron microscopy images at 21 days post eclosion, as compared to controls.
Scer\GAL4Bx-MS1096-mediated expression causes the loss or strong reduction of wings.
When fz2Scer\UAS.N is expressed in dorsal cluster neurons under the control of Scer\GAL4ato.3.6 the branching pattern in the adult medulla is disturbed, giving rise to an increased number of branches at the 3rd branching point of the grid-like structure.
Third instar larvae expressing fz2Scer\UAS.N under the control of Scer\GAL4Mhc.PU show a reduction in neuromuscular junction size compared to controls.
One copy of fz2Scer\UAS.N has no effect on hemocyte proliferation in third instar larvae.
Expression of fz2Scer\UAS.N under the control of Scer\GAL469B results in severely notched wings. Expression of fz2Scer\UAS.N in the anteroposterior wing boundary using Scer\GAL4dpp.blk1 results in a mild wing notching phenotype.
Expression of fz2Scer\UAS.N under the control of Scer\GAL4fkh.PZ results in salivary gland guidance defects; a large portion of the salivary gland curves towards the central nervous system, with the curving beginning early, as the gland migrates along the circular visceral mesoderm.
fz2Scer\UAS.N; Scer\GAL4sd-SG29.1 flies have highly reduced wings lacking all margin structures and much of the outer area of the wing blade.
When expressed from Scer\GAL4ptc-559.1 the apical cells of the ovarian sheath remain clustered in the apical region of the ovary, indicating that they are not capable of basal migration.
Expression of fz2Scer\UAS.N under the control of Scer\GAL4dpp.blk1 results in ectopic furrow formation in the eye disc.
Ectopic expression of fz2Scer\UAS.N at the presumptive wing margin using Scer\GAL4C96 is associated with a fully penetrant mild wing margin defect.
When expression is driven by Scer\GAL4hs.2sev, the two chiral forms of ommatidia are intermixed in the dorsal and ventral half of the eye. When expression is driven by Scer\GAL469B, significant wing margin and bristle loss occurs, with reduction in wing size. When expression is driven by Scer\GAL469B, ectopic wing bristle phenotype of fz2Scer\UAS.cZa is suppressed.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Enhancer of
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Additional Comments
Genetic Interactions
Statement
Reference
The reduction in neuromuscular junction size seen in third instar larvae expressing fz2Scer\UAS.N under the control of Scer\GAL4Mhc.PU is suppressed if they are also heterozygous for either LanA9-32 or βInt-ν1.
Expression of hipkScer\UAS.T:Ivir\HA1 in animals expressing fz2Scer\UAS.N under the control of Scer\GAL469B rescues the severely notched wing phenotype. Removing one copy of hipk4 in animals expressing fz2Scer\UAS.N in the anteroposterior wing boundary using Scer\GAL4dpp.blk1 enhances the wing notching phenotype, resulting in moderate to severely truncated wings.
Wing size reduction and loss of wing margin structures in fz2Scer\UAS.N; Scer\GAL4sd-SG29.1 flies is significantly suppressed by nmoDB24/nmoDB24.
The wing margin defect produced by expression of fz2Scer\UAS.N using Scer\GAL4C96 is strongly enhanced by dally06464/dally06464.
The phenotype caused by expression of fz2Scer\UAS.N using fz2Scer\UAS.N is slightly dominantly enhanced by heterozygosity for wgl-17.
Xenogenetic Interactions
Statement
Reference
One copy of fz2Scer\UAS.N moderately 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
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
fz2Scer\UAS.N
fz2UAS.N
Name Synonyms
Secondary FlyBase IDs
    References (16)