FlyBase Allele Report: Dmel\Rho1[N19.UAS]

Maternal expression of Rho1^N19.UAS under the control of Scer\GAL4^{VP16.mat.αTub67C} leads to severe epidermal and cuticle defects in the embryo, namely a large number of epithelial vesicles and lack of cuticle shields.

(Silver et al., 2019)

Expression of Rho1^N19.UAS under the control of Scer\GAL4^VP16.bam in testes leads to scattered spermatid nuclei and actin cones compared to controls.

(Steinhauer et al., 2019)

Expression of Rho1^N19.Scer\UAS in founder cells under the control of Scer\GAL4^kirre-rP298 disrupts myoblast fusion in wild type embryos. A more severe phenotype is seen in Rho1^72O 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 Rho1^72O mutant embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^kirre-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 Rho1^N19.Scer\UAS in fusion-competent myoblasts (FCMs) under the control of Scer\GAL4^sns.PK causes a less severe fusion defect.

(Kim et al., 2015)

Expression of Rho1^N19.Scer\UAS for 12 hours under the control of Scer\GAL4^P0.5.Pdf (restricted to the adult stages using Scer\GAL80^ts.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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^P0.5.Pdf (restricted to the adult stages using Scer\GAL80^ts.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).

(Petsakou et al., 2015)

Haemocytes bled from homozygous third instar larvae expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^srp.Hemo show a marked increase in the number of filopodia compared to control haemocytes.

(Bausek and Zeidler, 2014)

Scer\GAL4^btl.PS-mediated expression of Rho1^N19.Scer\UAS does not cause significant tracheal branching defects.

(Iordanou et al., 2014)

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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^NP2432.

(Taniguchi et al., 2011)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^dpp.blk1 induces ectopic apoptosis in third instar wing imaginal disc cells.

(Neisch et al., 2010)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^{nos.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.

(Renault et al., 2010)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^elav.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.

(Shuai et al., 2010)

Expression of Rho1^N19.Scer\UAS in R-cells under the control of Scer\GAL4^GMR.PF induces an axonal-hyperfasciculation phenotype.

(Yu et al., 2010)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^prd.RG1 results in deepened segmental grooves in the embryo.

(Homem and Peifer, 2009)

Animals carrying Rho1^N19.Scer\UAS, Scer\GAL4^ptc-559.1 and Scer\GAL80^ts.αTub84B which have been shifted to 29[o]C to inactivate Scer\GAL80^ts.αTub84B and allow expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^ptc-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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^ptc-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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^Act are rounded without the interdigitating borders usually seen in clones in pupal wings. The cells have an increased cross section and decreased F-actin.

(Yan et al., 2009)

Embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^fkh.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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^en-e16E show defects in salivary gland migration.

Salivary glands fail to turn and migrate properly in embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^twi.PB.

(Xu et al., 2008)

Expression of Rho1^N19.Scer\UAS in the border cells under the control of Scer\GAL4^slbo.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.

(Bastock and Strutt, 2007)

Overexpression of Rho1^N19.Scer\UAS in the hindgut epithelium under the control of Scer\GAL4^NP2432 causes left-right symmetry defects in the hindgut.

(Taniguchi et al., 2007)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^NP2432 results in synchronous left-right defects in the embryonic midgut and hindgut.

(Hozumi et al., 2006)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^ems.HRE, interferes with spiracle-cell invagination.

(Lovegrove et al., 2006)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^ems.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.

(Simões et al., 2006)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^ato.3.6 does not affect dorsal cluster neuron axon extension across the optic chiasm in adult flies.

(Srahna et al., 2006)

The tip cell stalks of Malpighian tubules that express Rho1^N19.Scer\UAS under the control of Scer\GAL4^ct.CtB are extended compared to wild-type stalks.

(Denholm et al., 2005)

Expression of Rho1^N19.Scer\UAS in sensory organ precursor cells, driven by Scer\GAL4^neur-P72, inhibits cytokinesis.

(Emery et al., 2005)

Embryos expressing Rho1^N19.Scer\UAS under the simultaneous control of both Scer\GAL4^Pxn.PS and Scer\GAL4^crq.PA recruit fewer than half the number of hemocytes to a laser-induced wound after one hour compared to wild type embryos. Most Rho1^N19.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 Rho1^N19.Scer\UAS-expressing cells appear to 'snap free' of their tails and leave a trail of membrane/cytoplasm behind them.

(Stramer et al., 2005)

Expression of Rho1^N19.Scer\UAS under the control of either Scer\GAL4^da.G32, Scer\GAL4^{Cg25C-A109.1F2.P} or Scer\GAL4^gcm-rA87.P does not alter migration, distribution or morphology of macrophages in the embryo.

(Paladi and Tepass, 2004)

Cytokinesis is blocked in Rho1^N19.Scer\UAS; Scer\GAL4^twi.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.

(Schumacher et al., 2004)

When Rho1^N19.Scer\UAS is overexpressed under the control of Scer\GAL4^elav.PLu, mutants do not exhibit longitudinal axon ectopic midline crossing defects

(Fan et al., 2003)

When Rho1^N19.Scer\UAS is driven by Scer\GAL4^{nos.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.

(Kunwar et al., 2003)

When Rho1^N19.Scer\UAS is driven by Scer\GAL4^repo 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.

(Sepp and Auld, 2003)

Embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^en-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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^prd.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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^prd.RG1 have apical filopodia and generally appear larger and more rounder than neighbouring wild-type cells. Some cells which express Rho1^N19.Scer\UAS under the control of Scer\GAL4^prd.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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^en-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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^prd.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 Rho1^N19.Scer\UAS under the control of Scer\GAL4^en-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.

(Bloor and Kiehart, 2002)

When Rho1^N19.Scer\UAS is driven by Scer\GAL4^ftz.ng, no midline crossovers are seen in the pCC/MP2 pathway axons. When Rho1^N19.Scer\UAS is driven by Scer\GAL4^elav.PLu, no adults eclose.

(Fritz and VanBerkum, 2002)

Expression of Rho1^N19.Scer\UAS driven by Scer\GAL4^332.3 does not affect either the dorsal cuticle or amnioserosa morphology.

(Harden et al., 2002)

Leading edge cells expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^en-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 Rho1^N19.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 Rho1^N19.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 Rho1^N19.Scer\UAS-expressing cells that clearly have a migration advantage over their wild-type, cable-assembling neighbors.

(Jacinto et al., 2002)

Cells in the tracheal dorsal trunk do not form a distinct lumenal cavity in embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^btl.PS, although cells in the dorsal trunk are continuous. Primary and secondary branching of the tracheal system appears normal.

(Lee and Kolodziej, 2002)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^c381 or Scer\GAL4^Kr.PM results in severe defects in germ band retraction. Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^pnr-MD237 affects dorsal closure but does not disrupt germ band extension or retraction.

(Schock and Perrimon, 2002)

When Rho1^N19.Scer\UAS is driven by Scer\GAL4^how-24B, embryonic muscle patterning is affected. Ventral longitudinal muscles are often seen to be missing. Muscle attachment however appears normal.

(Bloor and Kiehart, 2001)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^hs.PB (using heat shock) results in many embryos with holes in the dorsal surface.

(Harden et al., 1999)

60% of embryos expressing the dominant negative Rho1^N19.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.

(Lu and Settleman, 1999)

Expression of Rac1^N17.Scer\UAS under the control of Scer\GAL4^48Y in the developing midgut has no effect on the migration of the endodermal midgut cells.

(Martin-Bermudo et al., 1999)

Over expression of Rho1^N19.Scer\UAS driven by Scer\GAL4^prd.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.

(Prokopenko et al., 1999)

Scer\GAL4^twi.PG-mediated expression causes severe cuticle defects. Patches of mesodermal cells fail to invaginate, invaginations of the anterior midgut are blocked. Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}-mediated expression causes a block in ventral furrow formation and invagination, disruption in cell shape changes.

(Hacker and Perrimon, 1998)

Ventral furrow formation is initially delayed relative to cephalic furrow formation in embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^nos.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.

(Barrett et al., 1997)

Causes a tissue polarity defect when expressed in the wing using Scer\GAL4^dpp.blk1; hairs fail to point distally, and some multiple wing hairs are seen.

(Strutt et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhancer of

Statement

Reference

Scer\GAL4^elav-C155/Rho1^N19.UAS is a non-enhancer of abnormal neuroanatomy | heat sensitive phenotype of N^l1N-ts1

(Song and Giniger, 2011)

Suppressor of

Statement

Reference

Rho1^N19.UAS/Scer\GAL4^e22c is a suppressor of decreased cell number | embryonic stage phenotype of Ncra\QF^srpHemo, kay^DN.QUAS

(Belyaeva et al., 2022)

Rho1^N19.UAS/Scer\GAL4^332.3 is a suppressor | partially of majority die during embryonic stage phenotype of crb^GX24w-/crb^11A22, crb^Y10A

(Flores-Benitez and Knust, 2015)

Scer\GAL4^{VP16.nanos.UTR}/Rho1^N19.UAS is a suppressor of decreased cell number | germline clone | maternal effect | embryonic stage 15 phenotype of wun2^EP2650ex34, wun⁴⁹

(Renault et al., 2010)

Scer\GAL4^{VP16.nanos.UTR}/Rho1^N19.UAS is a suppressor of decreased cell number | germline clone | maternal effect | embryonic stage 16 phenotype of wun2^EP2650ex34, wun⁴⁹

(Renault et al., 2010)

Scer\GAL4^{VP16.nanos.UTR}/Rho1^N19.UAS is a suppressor of increased cell death | germline clone | maternal effect | embryonic stage phenotype of wun2^EP2650ex34, wun⁴⁹

(Renault et al., 2010)

Scer\GAL4^NP2225/Rho1^N19.UAS is a suppressor of abnormal neuroanatomy | embryonic stage phenotype of cv-c¹²⁶⁰

(Sato et al., 2010)

Rho1^N19.UAS, Scer\GAL4^FRT.Act5C, Scer\GAL80^αTub84B.PL is a suppressor of hyperplasia | conditional | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^FRT.Act5C, Scer\GAL80^αTub84B.PL

(Zeng et al., 2010)

Scer\GAL80^ts.αTub84B, Scer\GAL4^ap-md544, Rho1^N19.UAS is a suppressor of abnormal cell shape | conditional | third instar larval stage phenotype of BacA\p35^UAS.cHa, Dad^UAS.cTa, Scer\GAL4^ap-md544, Scer\GAL80^ts.αTub84B

(Widmann and Dahmann, 2009)

Rho1^N19.UAS, Scer\GAL4^elav.PLu is a suppressor of abnormal neuroanatomy phenotype of RhoGEF64C^EP3035, Scer\GAL4^elav.PLu

(Bashaw et al., 2001)

Other

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^dome-PG5, hop^Tum has lethal phenotype

(Bausek and Zeidler, 2014)

BacA\p35^UAS.cHa, Rho1^N19.UAS, Scer\GAL4^ap-md544, Scer\GAL80^ts.αTub84B has abnormal cell shape | conditional | third instar larval stage phenotype

(Widmann and Dahmann, 2009)

Rho1^N19.UAS, Scer\GAL4^ap-md544, trc^T453A.UAS.L has lethal phenotype

(He et al., 2005)

Rho1^N19.UAS, Scer\GAL4^elav.PLu, sli² has abnormal neuroanatomy phenotype

(Fan et al., 2003)

Rho1^N19.UAS, Scer\GAL4^ftz.ng, sli² has abnormal neuroanatomy phenotype

(Fan et al., 2003)

Phenotype Manifest In

Enhanced by

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^ftz.ng has dMP2 neuron phenotype, enhanceable by robo1¹

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS, Scer\GAL4^ftz.ng has vMP2 neuron phenotype, enhanceable by robo1¹

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS, Scer\GAL4^ftz.ng has pCC neuron phenotype, enhanceable by robo1¹

(Fritz and VanBerkum, 2002)

NOT Enhanced by

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^slbo.2.6 has border follicle cell phenotype, non-enhanceable by fz^RNAi.UAS, Scer\GAL4^slbo.2.6

(Bastock and Strutt, 2007)

Suppressed by

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^{VP16.mat.αTub67C} has embryonic epidermis | maternal effect phenotype, suppressible by cyst^UASp.R, Scer\GAL4^{VP16.mat.αTub67C}

(Silver et al., 2019)

Rho1^N19.UAS, Scer\GAL4^{VP16.mat.αTub67C} has embryonic/larval cuticle | maternal effect | embryonic stage phenotype, suppressible by cyst^UASp.R, Scer\GAL4^{VP16.mat.αTub67C}

(Silver et al., 2019)

Rho1^72O, Rho1^N19.UAS, Scer\GAL4^{kirre-rP298-G4} has myoblast phenotype, suppressible | partially by Fim^UAS.Venus, Scer\GAL4^{kirre-rP298-G4}

(Kim et al., 2015)

Rho1^N19.UAS, Scer\GAL4^GMR.PF has lamina | third instar larval stage phenotype, suppressible by PlexA^RNAi.UAS, Scer\GAL4^GMR.PF

(Yu et al., 2010)

Rho1^N19.UAS, Scer\GAL4^GMR.PF has eye photoreceptor cell | third instar larval stage phenotype, suppressible by PlexA^RNAi.UAS, Scer\GAL4^GMR.PF

(Yu et al., 2010)

Rho1^N19.UAS, Scer\GAL4^ems.HRE has posterior spiracle primordium phenotype, suppressible by RhoGEF64C^UAS.cBa, Scer\GAL4^ems.HRE

(Simões et al., 2006)

Rho1^N19.UAS, Scer\GAL4^en-e16E has embryonic/first instar larval cuticle phenotype, suppressible | partially by BacA\p35^UAS.cHa, Scer\GAL4^en-e16E

(Bloor and Kiehart, 2002)

NOT suppressed by

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^{VP16.mat.αTub67C} has embryonic epidermis | maternal effect phenotype, non-suppressible by cyst^N.UASp.R, Scer\GAL4^{VP16.mat.αTub67C}

(Silver et al., 2019)

Rho1^N19.UAS, Scer\GAL4^{VP16.mat.αTub67C} has embryonic/larval cuticle | maternal effect | embryonic stage phenotype, non-suppressible by cyst^N.UASp.R, Scer\GAL4^{VP16.mat.αTub67C}

(Silver et al., 2019)

Rho1^N19.UAS, Scer\GAL4^ems.HRE has posterior spiracle primordium phenotype, non-suppressible by RhoGEF64C^ΔC.UAS, Scer\GAL4^ems.HRE

(Simões et al., 2006)

Enhancer of

Statement

Reference

Rho1^N19.UAS, Scer\GAL4^ftz.ng is an enhancer of dMP2 neuron phenotype of Ggal\MLCK^ct.UAS, Scer\GAL4^ftz.ng

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS, Scer\GAL4^ftz.ng is an enhancer of vMP2 neuron phenotype of Ggal\MLCK^ct.UAS, Scer\GAL4^ftz.ng

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of vMP2 neuron phenotype of Sos^e49

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of pCC neuron phenotype of Sos^e49

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS, Scer\GAL4^ftz.ng is an enhancer of pCC neuron phenotype of Ggal\MLCK^ct.UAS, Scer\GAL4^ftz.ng

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of dMP2 neuron phenotype of robo1¹

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of vMP2 neuron phenotype of robo1¹

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of pCC neuron phenotype of robo1¹

(Fritz and VanBerkum, 2002)

Rho1^N19.UAS/Scer\GAL4^ftz.ng is an enhancer of dMP2 neuron phenotype of Sos^e49

(Fritz and VanBerkum, 2002)

NOT Enhancer of

Statement

Reference

Scer\GAL4^elav-C155/Rho1^N19.UAS is a non-enhancer of larval intersegmental nerve | heat sensitive phenotype of N^l1N-ts1

(Song and Giniger, 2011)

Scer\GAL4^elav-C155/Rho1^N19.UAS is a non-enhancer of larval intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of N^l1N-ts1

(Song and Giniger, 2011)

Suppressor of

Statement

Reference

Rho1^N19.UAS/Scer\GAL4^e22c is a suppressor of embryonic/larval plasmatocyte | embryonic stage | decreased number phenotype of Ncra\QF^srpHemo, kay^DN.QUAS

(Belyaeva et al., 2022)

Rho1^N19.UAS/Scer\GAL4^e22c is a suppressor of germ band phenotype of Ncra\QF^srpHemo, kay^DN.QUAS

(Belyaeva et al., 2022)

Rho1^N19.UAS/Scer\GAL4^332.3 is a suppressor | partially of embryo | dorsal closure stage phenotype of crb^GX24w-/crb^11A22, crb^Y10A

(Flores-Benitez and Knust, 2015)

Rho1^N19.UAS/Scer\GAL4^332.3 is a suppressor | partially of embryonic/first instar larval cuticle | embryonic stage phenotype of crb^GX24w-/crb^11A22, crb^Y10A

(Flores-Benitez and Knust, 2015)

Rho1^N19.UAS/Scer\GAL4^btl.PS is a suppressor | partially of embryonic/larval ganglionic tracheal branch phenotype of exp¹³⁵

(Iordanou et al., 2014)

Scer\GAL4^{VP16.nanos.UTR}/Rho1^N19.UAS is a suppressor of germline cell | germline clone | maternal effect | embryonic stage 15 phenotype of wun2^EP2650ex34, wun⁴⁹

(Renault et al., 2010)

Scer\GAL4^{VP16.nanos.UTR}/Rho1^N19.UAS is a suppressor of germline cell | germline clone | maternal effect | embryonic stage 16 phenotype of wun2^EP2650ex34, wun⁴⁹

(Renault et al., 2010)

Scer\GAL4^NP2225/Rho1^N19.UAS is a suppressor of larval dorsal multidendritic neuron ddaE | embryonic stage phenotype of cv-c¹²⁶⁰

(Sato et al., 2010)

Scer\GAL4^NP2225/Rho1^N19.UAS is a suppressor of dendritic tree | embryonic stage phenotype of cv-c¹²⁶⁰

(Sato et al., 2010)

Rho1^N19.UAS, Scer\GAL4^FRT.Act5C, Scer\GAL80^αTub84B.PL is a suppressor of adult Malpighian tubule | conditional | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^FRT.Act5C, Scer\GAL80^αTub84B.PL

(Zeng et al., 2010)

Scer\GAL80^ts.αTub84B, Scer\GAL4^ap-md544, Rho1^N19.UAS is a suppressor of wing disc | conditional | third instar larval stage phenotype of BacA\p35^UAS.cHa, Dad^UAS.cTa, Scer\GAL4^ap-md544, Scer\GAL80^ts.αTub84B

(Widmann and Dahmann, 2009)

Rho1^N19.UAS, Scer\GAL4^elav.PLu is a suppressor of axon phenotype of RhoGEF64C^EP3035, Scer\GAL4^elav.PLu

(Bashaw et al., 2001)

Other

Statement

Reference

BacA\p35^UAS.cHa, Rho1^N19.UAS, Scer\GAL4^ap-md544, Scer\GAL80^ts.αTub84B has wing disc | conditional | third instar larval stage phenotype

(Widmann and Dahmann, 2009)

Rho1^N19.UAS, Scer\GAL4^elav.PLu, sli² has larval longitudinal connective phenotype

(Fan et al., 2003)

Rho1^N19.UAS, Scer\GAL4^ftz.ng, sli² has larval longitudinal connective phenotype

(Fan et al., 2003)

Additional Comments

Genetic Interactions

Statement

Reference

Maternal co-expression of cyst^UASp.R and Rho1^N19.UAS under the control of Scer\GAL4^{VP16.mat.αTub67C} leads to embryonic cuticle defects that are similar to those induced by the expression of cyst^UASp.R alone, and milder than those induced by Rho1^N19.UAS alone. By contrast, the cuticle defects induced by the maternal expression of Rho1^N19.UAS are not modified by the co-expression of cyst^N.UASp.R.

(Silver et al., 2019)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^332.3 partially suppresses the embryonic lethality and dorsal closure defects seen in embryos expressing crb^Y10A in a crb^GX24w-/crb^11A22 background.

(Flores-Benitez and Knust, 2015)

Expression of Fim^{Scer\UAS.T:Avic\GFP-YFP.Venus} significantly rescues the myoblast fusion defects seen in Rho1^72O mutant embryos expressing Rho1^N19.Scer\UAS in founder cells under the control of Scer\GAL4^kirre-rP298.

(Kim et al., 2015)

Co-expression of cpa^{Scer\UAS.N.T:Ivir\HA1} and cpb^Scer\UAS.cWa in Rho1^N19.Scer\UAS overexpressing wing discs (all under the control of Scer\GAL4^sd-SG29.1) restores tissue growth and suppresses Mmp1 accumulation, as found in wing discs expressing Rho1^N19.Scer\UAS alone. However, co-expression of cpa^{Scer\UAS.N.T:Ivir\HA1} and cpb^Scer\UAS.cWa does not affect growth or ectopic Mmp1 expression.

(Fernández et al., 2014)

The ISNb bypass phenotype of N^l1N-ts1 mutant embryos is not significantly modulated by expression of Rho1^N19.Scer\UAS (under the control of Scer\GAL4^elav-C155).

(Song and Giniger, 2011)

Expression of Rho1^N19.Scer\UAS in the germline under the control of Scer\GAL4^{nos.UTR.T:Hsim\VP16} rescues the germ cell death seen in embryos derived from females carrying wun⁴⁹ wun2^EP2650ex34 germline clones. No germ cells can be detected outside of the gut.

(Renault et al., 2010)

Expression of Rho1^N19.Scer\UAS under the control of Scer\GAL4^NP2225 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.

(Sato et al., 2010)

The severity of the Rho1^N19.Scer\UAS axonal-hyperfasciculation phenotype is significantly suppressed by knockdown of plexA^{dsRNA.Scer\UAS} (with both transgenes under the control of Scer\GAL4^GMR.PF).

(Yu et al., 2010)

Hyperplasia in adult Malpighian tubule clones expressing Ras85D^V12.Scer\UAS (using the MARCM system, under the control of Scer\GAL80^αTub84B.PL and Scer\GAL4^{Scer\FRT.Act5C}) is suppressed by co-expression of Rho1^N19.Scer\UAS.

(Zeng et al., 2010)

Co-expression of fz^{dsRNA.Scer\UAS} in border cells expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^slbo.2.6 does not alter the border cell phenotype observed when Rho1^N19.Scer\UAS is expressed alone.

(Bastock and Strutt, 2007)

Co-expression of Gef64C^Scer\UAS.cBa rescues the invagination defects seen in the posterior spiracles of embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^ems.HRE, resulting in normal spiracular chamber formation in 73.8% of cases.

Co-expression of Gef64C^ΔC.Scer\UAS does not rescue the invagination defects seen in the posterior spiracles of embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^ems.HRE.

(Simões et al., 2006)

Coexpression of Rho1^N19.Scer\UAS and trc^{T453A.Scer\UAS} under the control of Scer\GAL4^ap-md544 induces synthetic lethality.

(He et al., 2005)

The combination of heterozygous sli² and pan-neural overexpression of Rho1^N19.Scer\UAS (expressed under the control of Scer\GAL4^elav.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 Rho1^N19.Scer\UAS is driven by Scer\GAL4^ftz.ng, 7.4 defects are seen per animal, and an average of 67% of segments have defects.

(Fan et al., 2003)

The addition of Rho1^N19.Scer\UAS (driven by Scer\GAL4^ftz.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 Rho1^N19.Scer\UAS (driven by Scer\GAL4^ftz.ng) to Sos^e49 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 chic^sand-1 to any of Rho1^N19.Scer\UAS embryos, has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons.

(Fritz and VanBerkum, 2002)

Co-expression of Rho1^N19.Scer\UAS strongly suppresses the gain of function axon guidance defects caused by expression of Gef64C^EP3035 under the control of Scer\GAL4^elav.PLu.

(Bashaw et al., 2001)

Xenogenetic Interactions

Statement

Reference

Co-expression of Rho1^N19.Scer\UAS and BacA\p35^Scer\UAS.cHa in the dorsal compartment of the wing disc (under the temperature-regulated control of Scer\GAL4^ap-md544 by Scer\GAL80^ts.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 Dad^Scer\UAS.cTa and BacA\p35^Scer\UAS.cHa (under the temperature-regulated control of Scer\GAL4^ap-md544 by Scer\GAL80^ts.αTub84B), is rescued by co-expression of Rho1^N19.Scer\UAS.

(Widmann and Dahmann, 2009)

The addition of Rho1^N19.Scer\UAS to Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.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.

(Fritz and VanBerkum, 2002)

Complementation and Rescue Data

Comments

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Mutant

Wild-type

Stocks (3)

Bloomington

7327

P{UAS-Rho1.N19}1.3, w^*

7328

w^*; P{UAS-Rho1.N19}2.1

58818

w^*; P{UAS-Rho1.N19}2/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (8)

Reported As

Symbol Synonym

Rho1.N19

(Taniguchi et al., 2011)

Rho1^DN

(Rosa-Birriel et al., 2024)

Rho1^N19.Scer\UAS

Rho1^N19.UAS

Rho1^N19

(Stramer et al., 2005)

Rho^DN

(Homem and Peifer, 2009)

RhoA^DN

(Greig and Bulgakova, 2020, Srahna et al., 2006)

RhoN19

(Homem and Peifer, 2009)

Name Synonyms

Secondary FlyBase IDs

References (98)

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