FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Rac1N17.hs
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General Information
Symbol
Dmel\Rac1N17.hs
Species
D. melanogaster
Name
FlyBase ID
FBal0042717
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Transgenic product class
Nature of the Allele
Transgenic product class
Progenitor genotype
Carried in construct
Cytology
Description

Expression of the mutated cDNA is driven by an Hsp70 promoter.

Allele components
Component
Use(s)
Regulatory region(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

Embryos expressing Rac1N17.hs show a failure of dorsal closure. This phenotype is suppressed by Rac1V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB.

Heat induced expression causes border cell migration to halted in 98% egg chambers. The actin cage that normally surrounds stage 11 nurse cell nuclei is absent resulting in ring canals becoming obstructed by the nuclei and failure to complete cytoplasm transfer.

Heat shock at intervals from 4-5 hours to 9-10 AEL produces high frequency of defects in dorsal closure due to disruption of cell shape changes in the lateral epidermis, accompanied by disruption of a localised accumulation of actin and myosin thought to be driving epidermal cell shape change. Embryos also exhibit defects in germband retraction and head involution.

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

The dorsal closure defects of embryos co-expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 4 to 8 hours after egg laying are more severe than the defects produced by expression of either Rac1N17.hs or Cdc42N17.Scer\UAS alone. In contrast, the defects produced by co-expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 8 to 12 hours after egg laying are weaker than Rac1N17.hs expressed alone, but stronger than Cdc42N17.Scer\UAS expressed alone. When Rac1N17.hs is co-expressed with Cdc42V12.Scer\UAS under the control of Scer\GAL4hs.PB most cuticles are extremely disrupted. There is evidence of some rescue of the Rac1N17.hs phenotype by Cdc42V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB, as there are greater numbers of wild-type and mild dorsal closure defective embryos than seen with the expression of Rac1N17.hs alone.

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

Dominant inhibitory form of Rac1.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Rac1N17.hs
Name Synonyms
Secondary FlyBase IDs
    References (4)