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General Information
Symbol
Dmel\Rho1N19.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0061659
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rho1N19, Rho1N19, UAS-RhoN19, UAS-RhoN19, UAS-Rho1.N19, UAS-RhoAN19, Rho1.N19, UASrhoN19, UAS-Rho1
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 dominant negative 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 ( 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

cortical actin cytoskeleton & embryonic posterior spiracle, with Scer\GAL4ems.HRE

Detailed Description
Statement
Reference

Expression of Rho1N19.Scer\UAS in founder cells under the control of Scer\GAL4kirre-rP298 disrupts myoblast fusion in wild type embryos. A more severe phenotype is seen in Rho172O mutant embryos.

In contrast to the round and dense morphology seen in wild type, the F-actin enriched-structures between unfused fusion-competent myoblasts and miniature myotubes in Rho172O mutant embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4kirre-rP298 are irregularly shaped and exhibit abnormally long invasive protrusions. Ribosomes and intracellular organelles are frequently observed within the abnormal protrusions. Fusion pores fail to form.

Expression of Rho1N19.Scer\UAS in fusion-competent myoblasts (FCMs) under the control of Scer\GAL4sns.PK causes a less severe fusion defect.

Expression of Rho1N19.Scer\UAS for 12 hours under the control of Scer\GAL4P0.5.Pdf (restricted to the adult stages using Scer\GAL80ts.αTub84B) significantly increases the spread of s-LNv projections at ZT24 (dawn) compared with controls. As in controls there are oscillations in the spread and axonal volume between dusk or dawn.

In contrast to controls, which adjust their morning and evening activity peaks to align with seasonal dawn and dusk, flies expressing Rho1N19.Scer\UAS under the control of Scer\GAL4P0.5.Pdf (restricted to the adult stages using Scer\GAL80ts.αTub84B) are active later than control flies when exposed to a summer light:dark cycle (14 hours day:10 hours night), and this is independent of activity levels. Timing of activity is unaffected compared to controls when the flies are exposed to a winter cycle (10 hours day:14 hours night). Normal locomotor activity is seen when the flies are kept in complete darkness (DD).

Haemocytes bled from homozygous third instar larvae expressing Rho1N19.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 Rho1N19.Scer\UAS does not cause significant tracheal branching defects.

Mutant hindgut epithelial cells do not show the left-right asymmetry in cell shape which is seen in wild-type hindgut epithelial cells at late stage 12 (before epithelial tube rotation) in embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4NP2432.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4dpp.blk1 induces ectopic apoptosis in third instar wing imaginal disc cells.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 blocks the transepithelial migration of germ cells leading the majority of germ cells to adhere to each other inside the midgut at late stages. The few germ cells that do manage to cross the gut epithelium are scattered in the soma at stage 16.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4elav.PU (using tub-Gal80[ts] to limit the expression to the adult stage) does not significantly alter 3 hr memory of adult flies in an aversive olfactory assay compared to controls.

Expression of Rho1N19.Scer\UAS in R-cells under the control of Scer\GAL4GMR.PF induces an axonal-hyperfasciculation phenotype.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4prd.RG1 results in deepened segmental grooves in the embryo.

Animals carrying Rho1N19.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 Rho1N19.Scer\UAS under the control of Scer\GAL4ptc-559.1 for 2-8 hours during the pupal stage have wings with a number of defects in hair formation; cells that do not form a hair, cells that appear delayed in hair formation, polyploid cells and occasional multiple hair cells are seen in pupal wings. Most hairs form at the distal most vertex/side of cells, but some appear to form at an alternative location and do not point distally. Regions of the wing that are expressing Rho1N19.Scer\UAS under the control of Scer\GAL4ptc-559.1 are thinner than neighbouring regions, with increased cell width and decreased cell height. In some cases, cells appear to be expelled from the epithelium.

Clones in the pupal wing expressing Rho1N19.Scer\UAS under the control of Scer\GAL4Act are rounded without the interdigitating borders usually seen in clones in pupal wings. The cells have an increased cross section and decreased F-actin.

Embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4fkh.PH show defects in salivary gland development; in some cases cells invaginate to form a tube, but in other cases there is a failure to invaginate.

Embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4en-e16E show defects in salivary gland migration.

Salivary glands fail to turn and migrate properly in embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4twi.PB.

Expression of Rho1N19.Scer\UAS in the border cells under the control of Scer\GAL4slbo.2.6 results in spreading out of the normally compact border cell cluster along the anterior-posterior axis. Trailing edges of the border cells fail to retract towards the cell bodies. Border cell migration is strongly delayed, and in any particular cluster, many cells never reach the nucleus.

Overexpression of Rho1N19.Scer\UAS in the hindgut epithelium under the control of Scer\GAL4NP2432 causes left-right symmetry defects in the hindgut.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4NP2432 results in synchronous left-right defects in the embryonic midgut and hindgut.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4ems.HRE, interferes with spiracle-cell invagination.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4ems.HRE impairs Filzkorper secretion and the invagination of spiracle cells. The uninvaginated spiracle cells have a disrupted cortical actin cytoskeleton at their apical side, while elongation of the basolateral membrane (which occurs in wild type) is still seen.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4ato.3.6 does not affect dorsal cluster neuron axon extension across the optic chiasm in adult flies.

The tip cell stalks of Malpighian tubules that express Rho1N19.Scer\UAS under the control of Scer\GAL4ct.CtB are extended compared to wild-type stalks.

Expression of Rho1N19.Scer\UAS in sensory organ precursor cells, driven by Scer\GAL4neur-P72, inhibits cytokinesis.

Embryos expressing Rho1N19.Scer\UAS under the simultaneous control of both Scer\GAL4Pxn.PS and Scer\GAL4crq.PA recruit fewer than half the number of hemocytes to a laser-induced wound after one hour compared to wild type embryos. Most Rho1N19.Scer\UAS-expressing hemocytes in the locality of the wound are polarized toward it, but are held back by cytoplasmic tethers and are abnormally elongated. Occasionally, very elongated Rho1N19.Scer\UAS-expressing cells appear to 'snap free' of their tails and leave a trail of membrane/cytoplasm behind them.

Expression of Rho1N19.Scer\UAS under the control of either Scer\GAL4da.G32, Scer\GAL4Cg25C-A109.1F2.P or Scer\GAL4gcm-rA87.P does not alter migration, distribution or morphology of macrophages in the embryo.

Cytokinesis is blocked in Rho1N19.Scer\UAS; Scer\GAL4twi.PB embryos. leading to the formation of multi-nucleated cells. This phenotype is fully penetrant. However, migration of mesodermal cells after invagination appears normal in these embryos.

When Rho1N19.Scer\UAS is overexpressed under the control of Scer\GAL4elav.PLu, mutants do not exhibit longitudinal axon ectopic midline crossing defects

When Rho1N19.Scer\UAS is driven by Scer\GAL4nos.UTR.T:Hsim\VP16 causes many germ cells to remain inside the posterior midgut of stage 10 embryos. Mutant germ-cells are clumped in the middle of embryos at stage 13. At stages 13-14, when wild-type cells assemble into gonads, very few mutant cells reach the gonad.

When Rho1N19.Scer\UAS is driven by Scer\GAL4repo the peripheral glia exhibit subtle phenotypes, with sensory axon defasciculation as a secondary effect. The vPG ce;; fails to separate from the main peripheral nerve branch at 26% (compared tp 9% in controls). ALl embryos die before the first larval stage.

Embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4en-e16E all have a large anterior hole, indicating a failure in head involution and have lateral scarring. About 40% of the embryos have a hole in the dorsal cuticle, indicating a disruption in dorsal closure and the rest show puckering at the dorsal midline. The embryos have small ventral holes and also have dorsal holes in the posterior part of the embryo. Embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4prd.RG1 all have a large anterior hole, indicating a failure in head involution and have lateral scarring. About 40% of the embryos have a hole in the dorsal cuticle, indicating a disruption in dorsal closure and the rest show puckering at the dorsal midline. The embryos also have wide ventral holes that extend laterally, frequently merging with the lateral defects. At the germband retraction stage, epidermal cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4prd.RG1 have apical filopodia and generally appear larger and more rounder than neighbouring wild-type cells. Some cells which express Rho1N19.Scer\UAS under the control of Scer\GAL4prd.RG1 have flattened and spread over each other and neighbouring wild-type cells. In stage 13 embryos prior to dorsal closure, leading edge cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4en-e16E have extensive filopodia. These leading edge cells appear to extend across the amnioserosa and continue to put out extensive filopodia as dorsal closure proceeds. When these filopodia come into contact they form ectopic lateral cell-cell adhesions and cell bridges. Leading edge cells undergoing germband retraction do not narrow dorsally (in contrast to wild type) bringing stripes of cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4prd.RG1 into close proximity and allowing filopodia to form ectopic cell "bridges" linking the stripes of cells. The leading edge cells appear to extend across the amnioserosa and continue to put out extensive filopodia as dorsal closure proceeds. Mesectodermal cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4en-e16E fail to invaginate at the ventral midline at stage 11 and instead spread along the midline groove created by the invagination of their wild-type neighbours.

When Rho1N19.Scer\UAS is driven by Scer\GAL4ftz.ng, no midline crossovers are seen in the pCC/MP2 pathway axons. When Rho1N19.Scer\UAS is driven by Scer\GAL4elav.PLu, no adults eclose.

Expression of Rho1N19.Scer\UAS driven by Scer\GAL4332.3 does not affect either the dorsal cuticle or amnioserosa morphology.

Leading edge cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4en-e16E fail to assemble an actin cable but do express broad filopodia and lamellipodia. Without a cable, they do not constrict at their leading (apical) edge in the way that their wild-type neighbors do. Subsequently, these Rho1N19.Scer\UAS-expressing stripes of cells sweep forward, apparently released from their usual constraints, overspilling and displacing their wild-type neighbors. Frequently, the dorsal edges of intervening wild-type stripes are enveloped by adjacent Rho1N19.Scer\UAS-expressing stripes, and this wild-type tissue is consequently trapped back from the leading edge. By the time that the dorsal hole is closed, most of the midline seam epithelium is taken up by Rho1N19.Scer\UAS-expressing cells that clearly have a migration advantage over their wild-type, cable-assembling neighbors.

Cells in the tracheal dorsal trunk do not form a distinct lumenal cavity in embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4btl.PS, although cells in the dorsal trunk are continuous. Primary and secondary branching of the tracheal system appears normal.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4c381 or Scer\GAL4Kr.PM results in severe defects in germ band retraction. Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4pnr-MD237 affects dorsal closure but does not disrupt germ band extension or retraction.

When Rho1N19.Scer\UAS is driven by Scer\GAL4how-24B, embryonic muscle patterning is affected. Ventral longitudinal muscles are often seen to be missing. Muscle attachment however appears normal.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4hs.PB (using heat shock) results in many embryos with holes in the dorsal surface.

60% of embryos expressing the dominant negative Rho1N19.Scer\UAS in the leading edge cells display a dorsal-open phenotype. All epidermal cells ultimately adopt an unstretched polygonal shape following a normal initial leading edge cell stretching at early stage 13.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL448Y in the developing midgut has no effect on the migration of the endodermal midgut cells.

Over expression of Rho1N19.Scer\UAS driven by Scer\GAL4prd.RG1 leads to the formation of polyploid cells. Almost every cell within the affected segments becomes binucleate, the cleavage furrow fails and cytokinesis is not initiated. This phenotype is worse than that associated with a loss of zygotic Rho1.

Scer\GAL4twi.PG-mediated expression causes severe cuticle defects. Patches of mesodermal cells fail to invaginate, invaginations of the anterior midgut are blocked. Scer\GAL4mat.αTub67C.T:Hsim\VP16-mediated expression causes a block in ventral furrow formation and invagination, disruption in cell shape changes.

Ventral furrow formation is initially delayed relative to cephalic furrow formation in embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4nos.PG, and the furrow, once formed does not extend at the posterior as far as in wild-type embryos. The anterior midgut fails to invaginate. Posterior midgut invagination is defective.

Causes a tissue polarity defect when expressed in the wing using Scer\GAL4dpp.blk1; hairs fail to point distally, and some multiple wing hairs are seen.

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

Scer\GAL4elav-C155/Rho1N19.UAS is a non-enhancer of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1

Suppressor of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
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Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4332.3 partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background.

Expression of FimScer\UAS.T:Avic\GFP-YFP.Venus significantly rescues the myoblast fusion defects seen in Rho172O mutant embryos expressing Rho1N19.Scer\UAS in founder cells under the control of Scer\GAL4kirre-rP298.

Co-expression of cpaScer\UAS.N.T:Ivir\HA1 and cpbScer\UAS.cWa in Rho1N19.Scer\UAS overexpressing wing discs (all under the control of Scer\GAL4sd-SG29.1) restores tissue growth and suppresses Mmp1 accumulation, as found in wing discs expressing Rho1N19.Scer\UAS alone. However, co-expression of cpaScer\UAS.N.T:Ivir\HA1 and cpbScer\UAS.cWa does not affect growth or ectopic Mmp1 expression.

The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Rho1N19.Scer\UAS (under the control of Scer\GAL4elav-C155).

Expression of Rho1N19.Scer\UAS in the germline under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 rescues the germ cell death seen in embryos derived from females carrying wun49 wun2EP2650ex34 germline clones. No germ cells can be detected outside of the gut.

Expression of Rho1N19.Scer\UAS under the control of Scer\GAL4NP2225 suppresses the reduction in length of secondary dendritic branches which is seen in the ddaE neurons of cv-c1260 embryos at 20-22 hours after egg laying.

The severity of the Rho1N19.Scer\UAS axonal-hyperfasciculation phenotype is significantly suppressed by knockdown of plexAdsRNA.Scer\UAS (with both transgenes under the control of Scer\GAL4GMR.PF).

Hyperplasia in adult Malpighian tubule clones expressing Ras85DV12.Scer\UAS (using the MARCM system, under the control of Scer\GAL80αTub84B.PL and Scer\GAL4Scer\FRT.Act5C) is suppressed by co-expression of Rho1N19.Scer\UAS.

Co-expression of fzdsRNA.Scer\UAS in border cells expressing Rho1N19.Scer\UAS under the control of Scer\GAL4slbo.2.6 does not alter the border cell phenotype observed when Rho1N19.Scer\UAS is expressed alone.

Co-expression of Gef64CScer\UAS.cBa rescues the invagination defects seen in the posterior spiracles of embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4ems.HRE, resulting in normal spiracular chamber formation in 73.8% of cases.

Co-expression of Gef64CΔC.Scer\UAS does not rescue the invagination defects seen in the posterior spiracles of embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4ems.HRE.

Coexpression of Rho1N19.Scer\UAS and trcT453A.Scer\UAS under the control of Scer\GAL4ap-md544 induces synthetic lethality.

The combination of heterozygous sli2 and pan-neural overexpression of Rho1N19.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) leads to longitudinal axon ectopic midline crossing defects. An average of 2 defects are seen per animal, and an average of 18% of segments have defects. If expression of Rho1N19.Scer\UAS is driven by Scer\GAL4ftz.ng, 7.4 defects are seen per animal, and an average of 67% of segments have defects.

The addition of Rho1N19.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 89% of embryos exhibit the phenotype. An average of 3.1 crossovers are seen per embryo. The addition of Rho1N19.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49 homozygous embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 94% of embryos exhibit the phenotype. An average of 7.0 crossovers are seen per embryo. The addition of chicsand-1 to any of Rho1N19.Scer\UAS embryos, has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons.

Co-expression of Rho1N19.Scer\UAS strongly suppresses the gain of function axon guidance defects caused by expression of Gef64CEP3035 under the control of Scer\GAL4elav.PLu.

Xenogenetic Interactions
Statement
Reference

Co-expression of Rho1N19.Scer\UAS and BacA\p35Scer\UAS.cHa in the dorsal compartment of the wing disc (under the temperature-regulated control of Scer\GAL4ap-md544 by Scer\GAL80ts.αTub84B) results in highly elongated apical-basal cell length in mutant cells compared with control cells.

The shorter cell length observed in wing disc tissue expressing DadScer\UAS.cTa and BacA\p35Scer\UAS.cHa (under the temperature-regulated control of Scer\GAL4ap-md544 by Scer\GAL80ts.αTub84B), is rescued by co-expression of Rho1N19.Scer\UAS.

The addition of Rho1N19.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 28% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo.

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