FB2024_03 , released June 25, 2024
Allele: Dmel\hhN.UAS
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General Information
Symbol
Dmel\hhN.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0045882
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-hhN, UAS-hh-N, UAS-HhN
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

UAS regulatory sequences drive expression of an N-terminal fragment (amino acid residues 1-257) of hh.

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 ( 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

Overexpression of hhN.Scer\UAS (under the regulation of Scer\GAL4en-e16E) results in conversion of tertiary fates (thick, pigmented hair) to ectopic secondary fates (smooth cuticle) on the dorsal epidermis of larvae.

When hhN.Scer\UAS is driven by Scer\GAL4unspecified the anterior wing is affected. Morphology and vein patterns are affected.

Scer\GAL4en-e16E-mediated expression causes grossly enlarged and misshapen wing discs.

Ectopic expression of hhN.Scer\UAS results in very similar phenotypes to those caused by ectopic expression of the full length protein, from hhhs.PI.

When expression is driven by Scer\GAL4en-e16E, ventral cuticle defects include a rectangular rather than a trapezoidal shape for the denticle belts and a loss of denticle diversity, and dorsal cuticle defects include a loss of tertiary and an expansion of secondary cell types. The phenotype is essentially identical to that caused by ubiquitous expression of a full length or N-truncated hh gene product.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The reduction in eye size seen in upd1unspecified/Df(1)os1A2 flies is increased by expression of hhN.Scer\UAS under the control of Scer\GAL4ey.PH and extra bristles are seen in the eye.

Overexpression of hhN.Scer\UAS under the regulation of Scer\GAL4en-e16E, in cos2 mutants fails to convert tertiary fates (thick, pigmented hair) to ectopic secondary fates (smooth cuticle) on the dorsal epidermis of larvae.

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

Feitz et al.

Comments
Comments

Expressed in S2 cells and used to produce conditioned medium containing hh protein to study its effect on ci-mediated transcriptional activation.

Carried in a plasmid and expressed in S2 cells. Used to produce a conditioned medium, which has been used to study the response of cl-8 cells to hh signalling.

Expressed in S2 cells.

Carried in a plasmid and transfected into S2 cells.

Carried in a plasmid and expressed in Schneider line 2 cells. The N cleavage product, in the absence of the C cleavage product.

Carried in plasmid "Hh-N", expressed in Schneider S2 cells that normally express fu and not hh to test the signalling from hh to fu in cultured cells.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
hhN.Scer\UAS
hhN.UAS
Name Synonyms
Secondary FlyBase IDs
    References (24)