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General Information
Symbol
Dmel\Rho1V14.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0105124
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rho1V14, UAS-RhoV14, UAS-RhoV14, UAS-RhoA V14, Rho1.V14, UAS-RhoAV14
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 constitutively active form of Rho1 is expressed under the control of UAS 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 ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
mushroom body & dendrite, with Scer\GAL4Tab2-201Y
mushroom body & dendrite | somatic clone, with Scer\GAL4Tab2-201Y
sensory neuron & axon, with Scer\GAL4repo
Detailed Description
Statement
Reference
Expressing Rho1Scer\UAS.cMa for 12 hours under the control of Scer\GAL4P0.5.Pdf (restricted to the adult stages using Scer\GAL80ts.αTub84B) increases the normally low number of dendrites in LNv projections at ZT2. Flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4P0.5.Pdf are arrhythmic.
Haemocytes bled from homozygous third instar larvae expressing Rho1V14.Scer\UAS under the control of Scer\GAL4srp.Hemo show a marked increase in the number of filopodia compared to control haemocytes.
Scer\GAL4btl.PS-mediated expression of Rho1V14.Scer\UAS causes fusion defects in the tracheal dorsal trunk and lateral trunk and extension defects in the ganglionic branch.
Flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a do not show significant neural vacuolization after 5 days as adults. Flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a do not perform well in a fast phototaxis assay but do not reveal significant neural vacuolization. Pan-neuronal expression of constitutively active Rho1V14.Scer\UAS (under the control of Scer\GAL4Appl.G1a) does not result in vacuoles in young (5 day old) flies. A few vacuoles are detectable in 14 day old flies, in contrast to age-matched controls. The total size and number of vacuoles are significantly increases in Rho1V14.Scer\UAS-expressing flies compared to controls. Expression of the constitutively active Rho1V14.Scer\UAS transgene in the developing eye under the control of Scer\GAL4GMR.PF results in dramatic nervous system degeneration in young flies. This affects the development of the retina, causing a smaller and severely rough eye. The retina is also much thicker in these mutants.
Expression of Rho1V14.Scer\UAS in motor neurons under the control of Scer\GAL4BG380 does not result in any neuromuscular junction overgrowth during larval development.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not block germ cell transepithelial migration or later germ cell migration.
Embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4btl.PS do not show defects in tracheal development.
Expression of Rho1V14.Scer\UAS in the dorsal compartment of the wing disc (under the temperature-regulated control of Scer\GAL4ap-md544 by Scer\GAL80ts.αTub84B) results in shorter cells compared with control cells.
Animals carrying Rho1V14.Scer\UAS, Scer\GAL4ptc-559.1 and Scer\GAL80ts.αTub84B which have been shifted to 29[o]C to inactivate Scer\GAL80ts.αTub84B and allow expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ptc-559.1 for 2-8 hours during the pupal stage show wings with cells that bulge apically, forming multiple wing hairs (the cells can have 10 or more short hairs) of relatively normal polarity. Most of the cells form hairs on the distal side, but some show hair formation at an alternative face/vertex, most often 60[o] from distal. The cells have increased cortical F-actin staining and decreased cytoplasmic actin staining. In some cases, cells appear to be expelled from the epithelium. Clones in the wing expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Act have an extreme multiple hair phenotype and a bulged cell surface.
Expression of Rho1V14.Scer\UAS in the border cells under the control of Scer\GAL4slbo.2.6 results in clusters with tightly rounded border cells and no large actin protrusions are observed. 50% of clusters show delays in migration.
Hemolymph clots from third instar larvae expressing Rho1V14.Scer\UAS under the control of Scer\GAL4He.PZ show a complete lack of melanization.
Stage 16 embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4ftz.ng display very few ventral nerve cord axon bundles that inappropriately cross the midline.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Gap1-NP3392 results in defects in the left-right asymmetry of the anterior midgut. 6% of embryos show inversion of the normal left-right asymmetry and 1% show no left-right asymmetry.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ems.HRE, interferes with spiracle-cell invagination.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ems.HRE blocks basolateral elongation and impairs cell invagination in the posterior spiracle. Very disorganised and superficially localised Filzkorper are formed in these embryos.
S2 cells expressing Rho1V14.Scer\UAS under the control of Scer\GAL4MtnA.PU adopt a contracted morphology.
Mutant germ cells successfully transmigrate the posterior midgut during stages 9 and 10 of embryogenesis, but subsequently some germ cells fail to move from the posterior midgut into the mesoderm.
When Rho1V14.Scer\UAS is driven by Scer\GAL4repo the peripheral glia do not migrate peripherally as normal, manifesting as dense clusters of glia arrested at their birth place at the CNS/PNS transition zone. Typically long actin containing fibres extend out of the glial clusters, and there are large expanses of PNS tracts with no glial sheaths whatsoever. The aberrant spike structures of the peripheral glia do not always project along sensory axon pathways. The lateral line glia fail to extend processes to interconnect between hemisegments and lateral chordotonal PNS glial cells appear collapsed and rounded, although their associated lateral chordotonal neurons appear properly formed. The sensory axon tracts in these mutants appear defasciculated although their pathfinding to the CNS is generally normal. The glial stalling phenotype is highly penetrant (97%).
Expression of Rho1V14.Scer\UAS, under the control of Scer\GAL4repo, in embryonic glia prevents extension of cytoplasmic processes and causes glial cell bodies to be stalled in the CNS-PNS transition zone. The distance between glia and sensory neuron birthplaces is much greater than the length of growth cones or their filopodial reach. Sensory axon pathways to the CNS are organized as in wild type, except that the axon tracts are defasciculated.
When Rho1V14.Scer\UAS is driven by Scer\GAL4ftz.ng, no midline crossovers are seen in the pCC/MP2 pathway axons. When Rho1V14.Scer\UAS is driven by Scer\GAL4elav.PLu, no adults eclose.
Leading edge cells expressing Rho1V14.Scer\UAS under the control of Scer\GAL4en-e16E are more constricted than their wild-type neighbors at early stages of dorsal closure. They subsequently take on irregular shapes and are outcompeted during dorsal closure, such that wild-type stripes tend to dominate the leading edge. Thus, when dorsal closure is complete, the midline seam epithelium is largely wild-type.
Lumen formation is blocked at all anastomosis sites in the tracheal system in embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4btl.PS. Tracheal branch migration is modestly attenuated but the pattern of primary and secondary branching is not detectably affected in these embryos.
A few adult escapers are seen at 18oC when Rho1V14.Scer\UAS is expressed under the control of Scer\GAL4OK107. These flies have complex mushroom body defects.
When driven by Scer\GAL4hs.2sev, Rho1V14.Scer\UAS flies show a loss of photoreceptors and misorientation of otherwise wild-type ommatidial clusters.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Tab2-201Y results in a 50% reduction in the volume of the dendritic field in the mushroom body neurons expressing Rho1V14.Scer\UAS. No abnormality in axonal projections is seen. There is no change in the total number of mushroom body neurons. When Rho1V14.Scer\UAS is expressed under the control of Scer\GAL4Tab2-201Y in a single mushroom body clone, the dendritic volume appears unaffected, but there is a 50% reduction of dendritic density. There is no change in the total number of mushroom body neurons.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
NOT suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Statement
Reference
Rho1V14.UAS/Scer\GAL460 is a non-enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Suppressor of
NOT Suppressor of
Additional Comments
Genetic Interactions
Statement
Reference
Expression of PuraGD12260 does not suppress the arrhythmicity seen in flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4P0.5.Pdf.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a decreases the performance index of SNF4Aγloe flies in a fast phototaxis assay. Expression of constitutively-active Rho1V14.Scer\UAS pan-neuronally, under the control of Scer\GAL4Appl.G1a, enhances the neural degeneration and vacuolization seen in SNF4Aγloe mutants. Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a decreases the performance index of SNF4Aγloe flies in a fast phototaxis assay. A SNF4Aγloe mutant background does not affect the external or internal eye phenotype caused by overexpression of Rho1V14.Scer\UAS under the control of Scer\GAL4GMR.PF. Overexpression of SNF4AγloeI.Scer\UAS under the control of Scer\GAL4GMR.PF suppresses the nervous system degeneration and vacuolization seen upon expression of Rho1V14.Scer\UAS.
Expression of Rho1V14.Scer\UAS fails to suppress the loss of F-actin rich protrusions seen in macrophages isolated from animals expressing SbfGD12081 under the control of Scer\GAL4Cg.PA.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4twi.PU partially rescues mesodermal cell morphology in pbl2/pbl3 embryos: cellular protrusions are not restored, but the defect in cell rounding is rescued.
The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Rho1V14.Scer\UAS (under the control of Scer\GAL460).
Expression of Rho1V14.Scer\UAS in the germline under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not rescue the germ cell death seen in embryos derived from females carrying wun49 wun2EP2650ex34 germline clones.
Co-expression of Rho1V14.Scer\UAS suppresses the dorsal cleft in the abdominal cuticle caused by expression of Atf3Scer\UAS.cSa under the control of Scer\GAL4ppl.PP.
Low levels of expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ptc-559.1 at 25[o]C (the flies also carry Scer\GAL80ts.αTub84B) partially suppress the mwh1/mwh6 multiple wing hair phenotype.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4twi.2PE does not enhance the mesodermal migration defects seen in pbl5 homozygotes.
Co-expression of fzdsRNA.Scer\UAS in border cells expressing Rho1V14.Scer\UAS under the control of Scer\GAL4slbo.2.6 ameliorates the rounded-border cell phenotype, and cells appear less round and produce actin-rich protrusions.
The frequency of crossovers across the midline in embryos expressing Rho1V14.Scer\UAS driven by Scer\GAL4ftz.ng is significantly increased by co-expression of fraScer\UAS.cKa. The frequency of crossovers across the midline in embryos expressing Rho1V14.Scer\UAS driven by Scer\GAL4ftz.ng is significantly increased by co-expression of fraΔP1.Scer\UAS. The frequency of crossovers across the midline in embryos expressing Rho1V14.Scer\UAS driven by Scer\GAL4ftz.ng is significantly increased by co-expression of fraΔP2.Scer\UAS. The frequency of crossovers across the midline in embryos expressing Rho1V14.Scer\UAS driven by Scer\GAL4ftz.ng is not increased by co-expression of fraΔP3.Scer\UAS. Co-expression of sqhT20A.S21A.Scer\UAS under the control of Scer\GAL4ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1V14.Scer\UAS and fraScer\UAS.cKa.
pucGS16811/+ has no effect on the defects in left-right asymmetry of the anterior midgut which are seen in embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Gap1-NP3392.
Rho1V14.Scer\UAS with Scer\GAL4twi.PB does not rescue the defects in mesodermal migration see in pblunspecified homozygous embryos.
The addition of Rho1V14.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 48% of embryos exhibit the phenotype. An average of 2.0 crossovers are seen per embryo. The addition of Rho1V14.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49 homozygous embryos suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 1.6% of embryos exhibit the phenotype. An average of 1.0 crossovers are seen per embryo. The addition of chicsand-1 to any of Rho1V14.Scer\UAS has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons.
Xenogenetic Interactions
Statement
Reference
When fraScer\UAS.cKa is co-expressed with both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng, all embryos exhibit severe defects in scaffold formation. Many ventral nerve cord axons either cross the midline or collapse into the midline region. Co-expression of sqhT20A.S21A.Scer\UAS under the control of Scer\GAL4ftz.ng suppresses the midline crossing phenotype in embryos expressing both Rho1V14.Scer\UAS and Ggal\MLCKct.Scer\UAS. The heterozygous Abl4-dependent suppression of the axonal midline crossing phenotype in embryos expressing Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng is lost if Rho1V14.Scer\UAS is also expressed.
The addition of Rho1V14.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 45% of embryos exhibit the phenotype. An average of 2.1 crossovers are seen per embryo.
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
Carried in plasmid "UAS-Rho1V14" and transfected into S2 cells with a driver construct.
Carried in plasmid "UAS-rhoV14", transfected into S2 cells and used to study the effect of the protein produced on actin and myosin organisation in the cells.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Rho1V14.Scer\UAS
Rho1V14.UAS
Name Synonyms
Secondary FlyBase IDs
    References (49)