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General Information
Symbol
Dmel\Rho172R
Species
D. melanogaster
Name
FlyBase ID
FBal0061660
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
RhoA72R
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Imprecise excision of the P{lacW} element, deleting part of the coding region, including the translation start site.
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
Heterozygotes show normal resistance to infection with P.aeruginosa by septic injury.
Rho172R mutant embryos exhibit a defect in tracheal invagination.
Clones of Rho172R in eye discs show malformed ommatidial preclusters.
Stage 17 Rho11B/Rho172R embryos show partial disruption of the cortical actin cytoskeleton in the spiracular chamber.
Rho172O/Rho172R embryos exhibit dramatic defects in head involution. None of these mutant embryos have a clear dorsal hole, although they frequently show puckering or segment misalignments along the closed midline seam. During dorsal closure lamellipodial and filopodial protrusions are more abundant at the leading edge than in wild-type, significantly increaing the total protrusive area of the leading edge. The cytoskeletal architecture typical of the leading edge is lost.
Laser wounded Rho172R/Rho172O embryos fail to assemble a continuous actin cable in wound-edge cells and there is little or no initial contraction of the leading edge of these cells. The leading-edge extends filopodia that are longer (extending up to 12 μm) and approximately three times more common than in wild-type embryos. In many instances, several filopodia coalesce to form a lamellipodium. Lamellipodia from adjacent leading-edge cells apparently tug on one another, resulting in the formation of several local zipping fronts around the wound margin, a behaviour only observed in wild-type in the last moments of wound closure, when opposing epithelial fronts are driven close enough together. Despite these differences with the wild-type, Rho172R/Rho172O embryos are able to close their wounds, but these take on average almost twice as long to repair as in their wild-type counterparts. There is a lag phase of nearly 2 hours (the time in which an equivalent wild-type wound can close fully) before the disorganized leading edge begins to move forward significantly. During this initial period, no obvious changes in cell shape occur in the leading-edge epithelial cells. However, once forward movement begins, the wound closes at a rate that is not significantly different to that of a wild-type wound (7.0+/-1.9 μm2/min; n = 6 in the mutant compared with 9.0+/-2.6 μm2/min; n = 5 in the wild type).
Mushroom body neuroblast clones homozygous for Rho172R consistently contain about 10-12 cells in third instar larvae (in contrast to wild-type mushroom body neuroblast clones which contain more than 150 neurons). Within each mutant clone, two of the nuclei are much larger than the rest of the nuclei. The clones project extensive dendrites in wandering third instar larvae that appear to occupy the entire calyx region. The effect on dendrite growth appears to be autonomous. In adulthood, mutant clones still contain 10-12 cells with axons projecting to only one medial lobe, in contrast to wild-type clones, which contain over 500 neurons that project axons to five lobes. Neurons of two cell or single cell mushroom body neuroblast clones homozygous for Rho172R and generated in newly hatched larvae have axon projections that are indistinguishable from wild type.
In homozygous mutant embryos, cytokinesis is blocked in affected cells. Many cells in the head region of the embryo become polyploid and contain two nuclei per cell. In addition polyploid cells are occasionally found in thoracic or abdominal segments of mutant embryos. Homozygous mutants have an "anterior open" phenotype.
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
Suppressor of
NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference
Rho172R/Rho1[+] is an enhancer of eye phenotype of CycEJP
NOT Enhancer of
Statement
Reference
Rho172R/Rho1[+] is a non-enhancer of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
Suppressor of
NOT Suppressor of
Statement
Reference
Rho172R/Rho1[+] is a non-suppressor of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
Rho172R is a non-suppressor of ommatidium phenotype of fz20/fz19
Additional Comments
Genetic Interactions
Statement
Reference
Rho172R/+ suppresses the ectopic apoptosis in wing disc cells expressing MoedsRNA.327-775.Scer\UAS under the control of Scer\GAL4dpp.blk1. Rho172R/+ strongly suppresses the Scer\GAL4dpp.blk1>MoedsRNA.327-775.Scer\UAS; pucE69/+ wing blade phenotype.
A Rho172R heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.
The Rho172R abnormal tracheal invagination phenotype is partially suppressed by cv-cM62.
Expression of shgdCR3h.Scer\UAS.T:Avic\GFP-rs under the control of Scer\GAL4hs.2sev in a Rho172R/+ background, enhances the ommatidial rotation phenotype of shgdCR3h.Scer\UAS.T:Avic\GFP-rs flies.
50% of cv-cM62 mutant embryos additionally homozygous for Rho172R and 20% of cv-cM62 mutant embryos heterozygous for Rho172R have a Malpighian tubule phenotype that is significantly less severe than that of the cv-cM62 homozygote alone. The tubules of double mutant embryos still undergo convergent extension movements to some extent.
Both hemizygous MoeG0323; Rho172R/+ and homozygous MoeG0323; Rho172R/+ adult retinas have normal photoreceptors.
The reduction in compartment size and the percentage of cells with multiple wing hairs in pbldsRNA.Scer\UAS; Scer\GAL4en-e16E flies are both enhanced by Rho172R/+.
Halving the maternal and zygotic dose of Rho1+ (using Rho172R) strongly suppresses the lethality of MoeG0323 animals and also suppresses the MoeG0323 disc epithelium organisation and actin localisation phenotypes.
When Rho172R fathers are crossed with Pkn06736 germline clone mothers, 68% of the embryos show a dorsal closure phenotype, an enhancement of the dorsal closure phenotype caused by Pkn06736 germline clones alone.
Rho172R dominantly suppresses the ommatidial, eye bristle, rhabdomere and pigment cell phenotypes seen in pblScer\UAS.cPa/Scer\GAL4GMR.PF flies to near wild-type. Rho172R dominantly enhances the ommatidial, eye bristle, rhabdomere and pigment cell phenotypes seen in pblΔDH497-549.Scer\UAS/Scer\GAL4GMR.PF flies.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments
Rho1Scer\UAS.cMa partially rescues the phenotype of homozygous Rho172R mushroom body neuroblast clones when expressed under the control of Scer\GAL4elav-C155.
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (25)