Open Close
General Information
Symbol
Dmel\RbfGMR.PD
Species
D. melanogaster
Name
glass multimer reporter construct of Du
FlyBase ID
FBal0048929
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
GMR-RBF4, GMRRBF4C
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

GMR regulatory sequences drive expression of a full length Rbf open reading frame.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Mutant animals exhibit fused ommatidia and missing interommatidial bristles.

Flies expressing RbfGMR.PD have a rough eye phenotype.

RbfGMR.PD flies with two copies of the responsible transposon, P{GMR-Rbf}, have no obvious phenotype in the eye. In flies with 4 copies of P{GMR-Rbf}, the posterior of the eye have missing bristles and pigment cells, and some fusion of ommatidia. Heat shock treatment of these flies has no affect on the phenotype. Treatment of RbfGMR.PD flies with four copies of P{GMR-Rbf} with the Nos inhibitor L-NAME (which does not affect eye morphology in wild-type flies) almost completely rescues the eye phenotype seen in these flies. The number of cells in S phase also increases.

Flies expressing RbfGMR.PD have a mild rough eye phenotype. The number of cells entering S phase posterior to the morphogenetic furrow is reduced compared to wild-type.

The eyes of adults carrying two copies of RbfGMR.PD are normal, four copies causes fused ommatidia and lack of bristles.

Flies carrying two copies of RbfGMR.PD transgene appear wild type, normal complement of retinal cells.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

RbfGMR.PD is a non-enhancer of visible phenotype of EBV\BZLF1GMR.PA

NOT Suppressor of
Statement
Reference

RbfGMR.PD is a non-suppressor of visible phenotype of EBV\BZLF1GMR.PA

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference

RbfGMR.PD, dapGMR.PdN has eye disc & S phase phenotype, suppressible by E2f1su89

RbfGMR.PD has ommatidium phenotype, suppressible by E2f1su89

RbfGMR.PD has eye phenotype, suppressible by ptcsu53/ptc[+]

RbfGMR.PD has phenotype, suppressible | partially by dapunspecified/dap[+]

RbfGMR.PD has phenotype, suppressible by CycDGMR.PE

RbfGMR.PD has eye phenotype, suppressible by DpGMR.PD/E2f1GMR.PD

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

RbfGMR.PD is a non-enhancer of eye phenotype of EBV\BZLF1GMR.PA

NOT Suppressor of
Statement
Reference

RbfGMR.PD is a non-suppressor of eye phenotype of EBV\BZLF1GMR.PA

Other
Additional Comments
Genetic Interactions
Statement
Reference

RbfGMR.PD when combined with dapGMR.PdN can inhibit or delay S phase entry during the second mitotic wave in developing eye disc. The introduction of E2fsu89 restores normal S phase entry in the second wave. dapGMR.PdN enhances the eye phenotype seen in dapGMR.PdN animals. These phenotypes are also suppressed by the addition of E2fsu89.

RbfGMR.PD, Noshs.PK flies, treated with heatshock before pupariation, lead to adults with multiple defects in the eye, including missing bristles and pigment cells. A lack of the regular number of pigment cells in these flies results in the appearance of many fused ommatidia and a rough eye phenotype. These phenotypes are seen in flies with to copies of the transposon responsible for RbfGMR.PD (P{GMR-Rbf}) and become more severe when 4 copies of P{GMR-Rbf} are present. RbfGMR.PD, NosGMR.PK flies have missing pigment and bristle cells and fused ommatidia. The addition of BacA\p35GMR.PH suppresses to wild-type the eye phenotype seen in E2fGMR.PD, DpGMR.PD, RbfGMR.PD flies. The inhibition of Nos activity with L-NAME prevents this suppression. The arrangement of ommatidia is still abnormal, and many additional pigment cells are still observed.

RbfGMR.PD; CycEJP double mutant flies have a more severe rough eye phenotype and greater reduction in the number of cells entering S phase posterior to the morphogenetic furrow than either RbfGMR.PD or CycEJP single mutant flies.

The mutant eye phenotype caused by RbfGMR.PD can be suppressed by coexpression of E2fGMR.PD and DpGMR.PD. RbfGMR.PD expression in adults carrying two copies of E2fGMR.PD and DpGMR.PD suppresses the rough eye phenotype, restoring the normal arrangement of ommatidia. CycEAR95 heterozygotes carrying four copies of RbfGMR.PD exhibit eyes with fused ommatidia and missing bristles.

Flies carrying a combination of dapGMR.PdN and RbfGMR.PD exhibit extremely rough eyes.

Xenogenetic Interactions
Statement
Reference

The eye phenotype of flies carrying a weakly expressing P{GMR-BZLF1.A} line is unaffected by RbfGMR.PD.

Complementation and Rescue Data
Comments
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
RbfGMR.PD
Name Synonyms
glass multimer reporter construct of Du
Secondary FlyBase IDs
    References (10)