Imprecise excision of the P{lacW} element, deleting part of the coding region, including the translation start site.
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 is an enhancer of visible | adult stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F is an enhancer of abnormal neuroanatomy | third instar larval stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F is an enhancer of abnormal neuroanatomy phenotype of DAAMEx68
Rho172F is an enhancer of partially lethal - majority die phenotype of DAAMEx1
Rho172F/Rho1[+] is a non-enhancer of abnormal neuroanatomy phenotype of DAAMEx1
Rho172F/Rho1[+] is a suppressor of abnormal phototaxis phenotype of SNF4Aγloe
Rho172F/Rho1[+] is a suppressor of abnormal neuroanatomy phenotype of SNF4Aγloe
Rho172F/Rho1[+], SNF4Aγloe has long lived phenotype
Df(3R)sbd105/+, Rho172F has visible | dominant phenotype
Rho172F has adherens junction | somatic clone phenotype, enhanceable by Rab11S25N.UASp.YFP/Scer\GAL4Act5C.PI
Rho172F has adherens junction | somatic clone phenotype, suppressible by Scer\GAL4Act5C.PI/Cdc42RNAi.UAS
Rho172F has adherens junction | somatic clone phenotype, suppressible by Scer\GAL4Act5C.PI/Rab5S43N.UASp.YFP
Rho172F has adherens junction | somatic clone phenotype, suppressible by Rab5GD10492/Scer\GAL4Act5C.PI
Rho172F has adherens junction | somatic clone phenotype, non-suppressible by Scer\GAL4Act5C.PI/diaCA.UAS.Tag:HA
Rho172F has adherens junction | somatic clone phenotype, non-suppressible by Scer\GAL4Act5C.PI/Rab5Q88L.UASp.YFP
Rho172F is an enhancer of eye phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F is an enhancer of eye disc | third instar larval stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F is an enhancer of axon | third instar larval stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F is an enhancer of larval brain | third instar larval stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Rho172F/Rho1[+] is an enhancer of retina phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Rho172F/Rho1[+] is an enhancer of ommatidium phenotype of Arf6GD13822, Dcr-2UAS.cDa, Scer\GAL4GMR.PF
Rho172F is an enhancer of connective phenotype of DAAMEx68
Rho172F is an enhancer of lateral longitudinal fascicle phenotype of DAAMEx68
Rho172F/Rho1[+] is an enhancer of retina | pupal stage P7 phenotype of Scer\GAL4GMR.PF, tkvRNAi.IR1.UAS, tkvRNAi.IR2.UAS
Rho172F/Rho1[+] is an enhancer of wing vein phenotype of Scer\GAL4sd-SG29.1, tkvRNAi.IR2.UAS
Rho172F/Rho1[+] is an enhancer of interommatidial precursor cell | pupal stage P7 phenotype of Scer\GAL4GMR.PF, tkvRNAi.IR2.UAS/tkvRNAi.IR1.UAS
Rho172F is an enhancer of embryonic/larval tracheal section phenotype of DAAMEx1
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 is a non-suppressor of embryonic/larval tracheal section phenotype of DAAMC.UASp, Scer\GAL4btl.PS
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 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.
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.
Rho172F is rescued by Scer\GAL4Act5C.PI/Rho1UAS.cMa
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.