FB2024_03 , released June 25, 2024
Allele: Dmel\kuzDN.UAS
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General Information
Symbol
Dmel\kuzDN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0062773
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-kuzDN, UAS-KUZ-DN, kuzDN
Key Links
Nature of the Allele
Progenitor genotype
Carried in construct
Cytology
Description

UASt regulatory sequences drive expression of a dominant-negative form of kuz. The Pro-domain and metalloprotease domain are deleted, leaving the SP, disintegrin domain, Cys-rich domain, transmembrane domain and intracellular domain intact.

Allele components
Component
Use(s)
Encoded product / tool
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

scutum & macrochaeta, with Scer\GAL432B

Detailed Description
Statement
Reference

Expression of kuzDN.Scer\UAS in the ap ipsilateral neurons under the control of Scer\GAL4ap-md544 causes ap neurons to ectopically cross the midline in approximately 15% of segments in stage 16 embryos.

Expression of kuzDN.Scer\UAS under the control of Scer\GAL4sca-109-68 results in duplication of the RP2 neurons.

Implantation of cells from Scer\GAL4sca-109-68 :kuzDN.Scer\UAS mutant embryos into wild-type embryos results in duplication of the aCC neuron at the expense of the pCC neuron as well as a loss of subperineural glia in NB1-1 lineages, duplication of the RP2 neuron at the expense of the RP2 sib as well as absence of the additional motor neurons in the NB4-2 lineage, duplication of the dMP2 cell in the MP2 lineage, and a complete absence of the U-neurons in the NB7-1 lineage.

Expression of kuzDN.Scer\UAS under the control of Scer\GAL4repo results in irregular peripheral glial cell migration in embryos.

Expression of kuzDN.Scer\UAS in border cells (under the control of Scer\GAL4slbo.2.6) suppresses border cell migration. This phenotype appears stronger at 29[o]C. The morphology of the border cells clusters is frequently different from wild-type. The clusters appear less round and the cells less tightly clustered.

Expression of kuzDN.Scer\UAS driven by Scer\GAL4twi.PG results in a hyperplasic heart, with the number of cardioblasts being increased approximately twofold. The number of pericardial cells appears to be reduced. The embryos also show severe muscle malformation defects.

Expression of kuzDN.Scer\UAS under the control of Scer\GAL4slbo.2.6 results in a severe impairment of border follicle cell migration. More than 90% of stage 10 egg chambers show delayed border cell migration, and border cells remain at the anterior tip of the egg chamber in 45% of cases.

Expression of kuzDN.Scer\UAS under the control of Scer\GAL4sim.PS results in no gross central nervous system (CNS) defects in 18% of embryos, while the remaining embryos have Fas2-positive axons crossing the midline. 40% of these embryos have a robo-like axon phenotype. The formation of the lateral Fas2-positive fascicle is affected. Muscle fibres are seen to cross the CNS dorsally.

When expression is driven by Scer\GAL432B, extra wing vein material develops in the wing, most notably forming deltas where the vein reaches the wing margin, the eyes are small and rough and extra bristles form on the notum.

Scer\GAL4elav-C155-mediated expression cause major defects in axonal pathways, such as disruption of longitudinal axonal tracts.

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

Scer\GAL432B, kuzDN.UAS has wing phenotype, non-suppressible by N+tCos479

Scer\GAL432B, kuzDN.UAS has wing vein phenotype, non-suppressible by N+tCos479

Scer\GAL432B, kuzDN.UAS has eye phenotype, non-suppressible by N+tCos479

Scer\GAL432B, kuzDN.UAS has scutum & macrochaeta phenotype, non-suppressible by N+tCos479

Enhancer of
Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference

Expression of kuzDN.Scer\UAS in ipsilateral ap neurons under the control of Scer\GAL4ap-md544 in a sli2/+ mutant background produces more severe ap axon midline crossing defects in stage 16 embryos than in either mutant alone.

One copy of robounspecified enhances the ectopic midline crossing phenotype seen when kuzDN.Scer\UAS is expressed in the ipsilateral ap neurons of stage 16 embryos under the control of Scer\GAL4ap-md544.

Expression of kuzDN.Scer\UAS in the ipsilateral ap neurons under the control of Scer\GAL4ap-md544 enhances the ectopic midline crossing phenotype seen in robounspecified/+ stage 16 embryos.

Co-expression of Nint.G.Scer\UAS with kuzDN.Scer\UAS in egg chamber border cells (under the control of Scer\GAL4slbo.2.6) ameliorates the migration defect observed in kuzDN.Scer\UAS mutants.

The phenotypes caused by expression of kuzDN.Scer\UAS driven by Scer\GAL432B are suppressed by three copies of wild type Dl, but not by N+tCos479.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Protein functions in a dominant negative manner.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
kuzDN.Scer\UAS
kuzDN.UAS
Name Synonyms
Secondary FlyBase IDs
    References (16)