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General Information
Symbol
Dmel\Rac1L89.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0038992
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-RacL89, UAS-RacL89, UAS-Rac1L89
Key Links
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

A dominant-negative form of Rac1 (carries the amino acid replacement S89L) is expressed under the control of UASt regulatory sequences.

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 ( 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

Expression of Rac1L89.Scer\UAS driven by Scer\GAL4slbo.2.6 results in the impairment of border cell migration during egg chamber development.

Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4Mef2.5xCD results in a small number of unfused myoblasts in the embryo.

Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4GMR.PF results in severe defects in the R-cell projection pattern in the optic lobe.

Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4ems.HRE eliminates the spiracular chamber.

Most salivary gland cells invaginate in embryos expressing Rac1L89.Scer\UAS under the control of Scer\GAL4fkh.PH, forming a tube with a slightly expanded lumen compared to wild type. At the stage when wild-type salivary gland cells turn to migrate posteriorly, the mutant lumen is thinner at its midpoint than normal or is completely broken, while the gland proper remains intact. At later stages, the salivary gland proper separates into pieces in the mutant embryos, with one segment at the surface of the embryo and another piece internal. 100% of stage 14 mutant embryos show this broken salivary gland phenotype.

Expression of Rac1L89.Scer\UAS in border cells, driven by Scer\GAL4slbo.2.6, inhibits the migration of border cell clusters to the oocyte. However, the apical cap of these egg chambers forms and is shed normally.

Embryos expressing Rac1L89.Scer\UAS under the control of Scer\GAL4gcm-rA87.P show a delay in macrophage migration; mutant embryos have a larger macrophage free area ventrally at stage 13 than wild-type embryos, and a ventral region devoid of macrophages also persists at later stages in the mutant embryos.

Expression of Rac1L89.Scer\UAS under the control of Scer\GAL4Cg25C-A109.1F2.P causes some clustering of macrophages at stage 17 and they extend more prominent cellular protrusions than normal.

Rac1L89.Scer\UAS driven by Scer\GAL4repo produces embryos that show ectopic lamellar like projections as well as failed inter-connection of the lateral line glia. The underlying sensory axonal tracts defasciculate. Misplacements od sensory appear to be associated with glia.

When expression is driven by Scer\GAL454 the eye is deformed.

Expression of Rac1L89.Scer\UAS by Scer\GAL4prd.RG1 has no effect on cytokinesis or mitosis.

Scer\GAL4elav-C155-mediated expression causes early ISNb growth cone arrest, axons never reach distal muscle targets. Scer\GAL4elav-C155-mediated expression slightly disrupts CNS axon pathway, gaps between segments suggest failure in axon extension. Coexpression of Rac1Scer\UAS.cLa under the same Scer\GAL4 driver causes a massive failure in axon extension, dramatically enhancing the effect of Rac1L89.Scer\UAS. Axons that do extend follow abnormal trajectories.

Only 15% embryos die when in combination with Scer\GAL4elav.PLu, surviving adults are completely viable. When in combination with Scer\GAL41407 one copy of Rac1L89.Scer\UAS causes some axonal loss between the lateral and dorsal clusters, two copies causes greater loss. One copy of Rac1Scer\UAS.cLa ameliorates this axonal loss. Scer\GAL4how-24B causes excessive fusion of the segmentally repeated myoblast cells.

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

Co-expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP with Rac1L89.Scer\UAS driven by Scer\GAL4slbo.2.6 enhances the border follicle cell migration phenotype associated with Rac1L89.Scer\UAS expression.

The R-cell axon projection defects caused by expression of Rac1L89.Scer\UAS under the control of Scer\GAL4GMR.PF are enhanced by bure10/+.

The salivary gland defects seen in embryos expressing Rac1L89.Scer\UAS under the control of Scer\GAL4fkh.PH are strongly suppressed by shg2/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (4)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Symbol Synonym
Rac1L89.Scer\UAS
Rac1L89.UAS
Rac1L89
Name Synonyms
Secondary FlyBase IDs
  • FBal0038991
References (18)