FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Rho172F
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General Information
Symbol
Dmel\Rho172F
Species
D. melanogaster
Name
FlyBase ID
FBal0061663
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
RhoA72F
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Imprecise excision of the P{lacW} element, deleting part of the coding region, including the translation start site.

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 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Heterozygous Rho172F flies do not show significant neural vacuolization after 5 days as adults.

Heterozygous Rho172F flies perform well in a fast phototaxis assay.

Rho172F/Rho172O stage 16 embryos have longer dorsal trunks than normal.

F-actin localisation at the level of the adherens junctions is disrupted in Rho172F homozygous clones.

Homozygous Rho172F mutants exhibit CNS defects in less than 10% of embryos.

The Rho172F mutation arrests tracheal development before dorsal trunk fusion takes place.

Rho172F/Rho172O, Rho172F/Rho172R and Rho172R/Rho172O embryos have an "anterior open" phenotype; the epidermis fails to close in the dorsal/anterior region. Rarely, the dorsal epidermis also fails to close. Some head structures are missing.

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

Rho172F/Rho1[+] is a non-enhancer of abnormal neuroanatomy phenotype of DAAMEx1

Rho172F/Rho1[+] is a non-enhancer of visible | recessive phenotype of Rab2351

Suppressor of
Statement
Reference

Rho172F/Rho1[+] is a suppressor of abnormal phototaxis phenotype of SNF4Aγloe

Rho172F/Rho1[+] is a suppressor of abnormal neuroanatomy phenotype of SNF4Aγloe

NOT Suppressor of
Statement
Reference

Rho172F/Rho1[+] is a non-suppressor of visible | recessive phenotype of Rab2351

Other
Phenotype Manifest In
Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

Rho172F is an enhancer of connective phenotype of DAAMEx68

Rho172F is an enhancer of embryo phenotype of DAAMEx68

Rho172F is an enhancer of neuropil phenotype of DAAMEx68

Rho172F is an enhancer of fascicle phenotype of DAAMEx68

NOT Enhancer of
Statement
Reference

Rho172F/Rho1[+] is a non-enhancer of adult mushroom body alpha-lobe phenotype of DAAMEx1

Rho172F/Rho1[+] is a non-enhancer of adult mushroom body beta-lobe phenotype of DAAMEx1

Rho172F/Rho1[+] is a non-enhancer of wing hair phenotype of Rab2351

Suppressor of
Statement
Reference

Rho172F/Rho1[+] is a suppressor of vacuole phenotype of SNF4Aγloe

NOT Suppressor of
Statement
Reference

Rho172F/Rho1[+] is a non-suppressor of wing hair phenotype of Rab2351

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

One copy of Rho172F does not enhance the axonal growth defects seen in the α and β lobes of DAAMEx1 mutant mushroom bodies.

Rho172F heterozygosity increases the performance index of SNF4Aγloe flies in a fast phototaxis assay.

Rho172F/+; SNF4Aγloe/SNF4Aγloe flies show a significant increase in lifespan compared to SNF4Aγloe mutants.

A heterozygous Rho172F background suppresses the neuronal vacuolization seen in SNF4Aγloe mutants to approximately half the level in single mutants. The number of vacuoles is also reduced, compared to SNF4Aγloe single mutants.

Heterozygosity for Rho172F enhances the patterning defects in the retina of flies co-expressing Arf51FGD13822 with Dcr-2Scer\UAS.cDa under the control of Scer\GAL4GMR.PF.

F-actin projections in the posterior region of Rho172F/+ ; RpII140wimp/+ stage 10b oocytes are reduced compared to wild-type oocytes.

Rho172F does not exhibit dominant genetic interaction with Rab2351.

Rho172F clones expressing diaCA.Scer\UAS.T:Ivir\HA1 still exhibit disrupted adherens junctions.

Expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172F clones enhances the Rho1 mutant phenotype. In addition to frequent disruptions to adherens junctions between clonal cells, there is also disruption of adherens junctions between clonal and wild-type cells.

Cdc42dsRNA.Scer\UAS expression suppresses the adherens junctions defects observed between two Rho172F cells but does not suppress the increased apical area.

Expression of Rab5S43N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172F clones suppresses the adherens junction defect seen between two Rho172F cells, although decreased apical tension is not affected.

Expression of Rab5Q88L.Scer\UAS.P\T.T:Avic\GFP-YFP (under the control of Scer\GAL4Act5C.PI) in Rho172F clones does not worsen the Rho172F adherens junction phenotype between two clonal pigment epithelial cells but does disrupt adherens junctions between a pigment epithelial cell and cone cell, a phenotype that is not found in Rho172O clones.

Expression of Rab5GD10492 in Rho172F clones suppresses the adherens junction defect seen between two Rho172F cells, although decreased apical tension is not affected.

Expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172F clones enhances the Rho1 mutant phenotype. In addition to frequent disruptions to adherens junctions between clonal cells, there is also disruption of adherens junctions between clonal and wild-type cells.

A Rho172F heterozygous background weakly enhances the zygotic DAAMEx68 CNS phenotype.

The frequency of inter-ommatidial pattering defects in tkvIR1.Scer\UAS; tkvIR2.Scer\UAS; Scer\GAL4GMR.PF pupal retinas at 42 hours APF is significantly enhanced by Rho172F/+.

The wing vein thickening phenotype seen in tkvIR2.Scer\UAS; Scer\GAL4sd-SG29.1 adults is enhanced by Rho172F/+.

The tracheal cuticle and semi-lethal phenotypes of DAAMEx1 larvae is enhanced by Rho172F.

Rho172F does not modify the effect of Scer\GAL4btl.PS>DAAMC.Scer\UAS.P\T expression on the larval trachea.

Rho172F shows a strong interaction (at least 50% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b and Sb70. Rho172F shows a weak interaction (5-24% of double heterozygotes have at least one malformed leg) with the following mutations: Df(3R)sbd105.

96% of Rho172F/zipEbr double heterozygotes have a malformed leg phenotype. Wing defects are also seen. Weak phenotypes include a broadening of the wing blade and folding back of the distal portion of the wing blade. In more severe cases, wings lacking adhesion between the wing blade bilayer and any apparent wing venation are seen. 17% of Rho172F/Df(2R)Jp1 double heterozygotes show a malformed phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Rho172F clones are rescued by expression of Rho1Scer\UAS.cMa. In some cases, a decrease in the apical area is observed, perhaps due to the high level of Rho1Scer\UAS.cMa overexpression.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (23)