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General Information
Symbol
Dmel\Rac1V12.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0038997
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rac1V12, UAS-RacV12, UAS-dRac1V12, UAS-RacV12, UAS-Rac1V12, UAS-Drac1(V12), RacV12, UAS-DracV12, UASDrac1V12, UAS-Drac1V12
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 Rac1 (carries the amino acid replacement G12V) is expressed under the control of UASt 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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
actin filament & border follicle cell | somatic clone, with Scer\GAL4Act5C.PI
axon & dorsal cluster neuron, with Scer\GAL4ato.3.6
Detailed Description
Statement
Reference
Third instar larvae expressing Rac1V12.UAS under the control of Scer\GAL4elav-C155 display supernumerary mature and satellite NMJ boutons.
The adulthood-only expression of Rac1V12.Scer\UAS under the combined control of Scer\GAL4ey-OK107 and Gal80[ts] leads to a severe decrease in intermediate-term olfactory memory (3h after conditioning), as compared to controls.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4GMR13F02 (in combination with a Gal80[ts] transgene to restrict expression to the adult stage) results in decreased memory after conditioning in an olfactory conditioning assay.
Expression of Rac1V12.Scer\UAS driven by Scer\GAL4hs.2sev causes defects in ommatidial rotation (planar cell polarity-like defects) and R-cell loss in the adult eye.
Adult mushroom body specific (using Scer\GAL4Mef2.247.Switch adults fed mifepristone/RU486) Rac1V12.Scer\UAS knockdown causes loss of acquired ethanol preference, as is seen in wild type (show increased ethanol consumption over 4 days); mutant flies have normal naive ethanol preference.
The mushroom body axons of flies expressing Rac1V12.Scer\UAS under the control of Scer\GAL4ey-OK107 fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype). Scer\GAL4ey-OK107>Rac1V12.Scer\UAS expressing clones that exhibit the posterior arrest phenotype display ectopic regions of F-actin in the posteriorly arrested axons.
Scer\GAL4btl.PS-mediated expression of Rac1V12.Scer\UAS severely disrupts tracheal development.
Scer\GAL4sns.PK-mediated expression of Rac1V12.Scer\UAS results in detached muscles in embryos.
Primary macrophages isolated from animals expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Cg.PA have an excess number of F-actin rich protrusions compared to wild type.
Expression of the constitutively active Rac1V12.Scer\UAS driven by Scer\GAL4sev.EP results in a normal eye phenotype.
Flies with induced expression of Rac1V12.Scer\UAS under the control of Scer\GAL4elav-C155 and Scer\GAL80ts.αTub84B do not display enhanced stress resistance compared to wild-type and exhibit diminished survival rates in high temperatures and when under paraquat-induced oxidative stress, compared to controls. A shortened life span is observed after continuous expression of Rac1V12.Scer\UAS for three days under the control of Scer\GAL4elav-C155 and Scer\GAL80ts.αTub84B (with flies kept at 30[o]C).
Expression of Rac1V12.Scer\UAS under the control of the neuronal drivers Scer\GAL4BG380, Scer\GAL4OK6 or Scer\GAL4elav-C155 leads to neuromuscular junction overgrowth during larval development, resulting in an increase in the number of synaptic boutons, branches and the appearance of abnormal synaptic protrusions. No overgrowth is seen when Rac1V12.Scer\UAS is expressed in muscle under the control of the Scer\GAL4Mhc.PW driver.
Expression of Rac1V12.Scer\UAS in the haemocytes under the control of Scer\GAL4crq.PO results in a failure of haemocyte migration into the posterior half of the embryo. These embryos also display a failure of anterior Malpighian tubule migration into the anterior half of the embryo. In these animals, the anterior pair of tubules projects into the posterior half of the embryo.
Expression of Rac1V12.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.
Conditional expression of Rac1V12.Scer\UAS under the control of Scer\GAL4ey-OK107 (using tub-Gal80[ts] to limit the expression to the adult stage) results in accelerated memory decay compared to controls although the immediate memory (3 and 15 in after training) is not affected. The sensimotor responses or mushroom body morphology are also not impaired. The Rac1V12.Scer\UAS expressing flies perform better compared to controls in an reversal learning aversive olfactory assay (in which the odor-shock contingency is reversed in each training session).
Expression of Rac1V12.Scer\UAS in the mesoderm under the control of Scer\GAL4twi.2PE results in mesoderm migration defects.
Stage 16 embryos overexpressing Rac1V12.Scer\UAS driven by Scer\GAL4ftz.ng display axon bundles that cross the midline inappropriately.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4srp.Hemo results in a 100% pentrant absence of haemocytes from the abdomen at 24 hours APF.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4Gap1-NP3392 results in defects in the left-right asymmetry of the anterior midgut. 13% of embryos show inversion of the normal left-right asymmetry and 5% show no left-right asymmetry.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4ems.HRE eliminates the spiracular chamber.
Expression of Rac1V12.Scer\UAS, under the control of Scer\GAL4ato.3.6, induces premature and severe retraction of dorsal cluster neuron axons visible even at L3.
When Rac1V12.Scer\UAS is expressed in the caudal visceral mesoderm (CVM) cells under the control of Scer\GAL4447.2 they fail to migrate towards the anterior pole of the embryo. The CVM cells remain viable at the posterior end of the embryo, indicating that cell survival is unaffected. Expression of vavΔ1-207.Scer\UAS.T:Ivir\HA1 under the control of the tracheal system driver Scer\GAL4btl.PS results in a variety of defects in the embryo including truncation of the tracheal dorsal trunk in some segments and severely misguided dorsal branching.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4wg.PM does not block cuticle secretion in embryos, but instead causes excess specification of denticles.
Expression of Rac1V12.Scer\UAS in border cells, driven by Scer\GAL4slbo.2.6, causes a border cell cluster migration defect in over 50-60% of egg chambers. However, the apical cap of these egg chambers forms and is shed normally.
Expression of Rac1V12.Scer\UAS, under the control of the hemocyte-specific driver Scer\GAL4crq.PO, inhibits hemocyte migration in the embryo by stage 14. Hemocytes begin migration out of the head region, but then lose polarized migration and accumulate in the anterior of the embryo. At stage 17, the ventral nerve cord is shorter in Rac1V12.Scer\UAS embryos than in wild-type, indicating that the VNC fails to condense correctly in Rac1V12.Scer\UAS mutants. Expression of Rac1V12.Scer\UAS in the lateral glia, driven by Scer\GAL4158, results in inhibition of VNC condensation in embryos but does not affect the pattern of axon tracts within the VNC. The differentiation and survival of the lateral glial cells are also unaffected. Expression of Rac1V12.Scer\UAS throughout the CNS, driven by Scer\GAL4elav-C155, inhibits VNC condensation and disrupts the pattern of axon tracts within the VNC.
Expression of Rac1V12.Scer\UAS in segmental stripes of the embryonic epithelium, driven by Scer\GAL4en-e16E, allows the embryo to survive to the dorsal closure stage. The leading edge cells of these embryos show produce larger lamellipodia than wild-type cells and appear to have a migrational advantage over neighbouring wild-type cells, so that the Scer\GAL4en-e16E stripes fuse with one another, resulting in almost all of the leading edge expressing Rac1V12.Scer\UAS. This leads to premature termination of dorsal closure, leaving a large hole in the dorsal epithelium.
When Rac1V12.Scer\UAS is driven by Scer\GAL4hs.PB (and heat shock) excessive contraction of the amnioserosa is seen. Also loss of cuticle secretion is seen.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4slbo.2.6 results in severe defects in border follicle cell migration.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4gcm-rA87.P blocks macrophage migration in embryos; most macrophages are unable to migrate and remain clustered anteriorly. Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4Cg25C-A109.1F2.P causes strong clustering of macrophages in the embryo, resulting in large regions of the embryo that are devoid of macrophages at stage 17. The macrophages extend longer, more prominent cellular protrusions than in wild type, and have a more elongated, spindle-like shape than in control embryos. Macrophages expressing Rac1V12.Scer\UAS under the control of Scer\GAL4unspecified show strongly elevated levels of cortical F-actin compared to wild type. The macrophages that cluster around the foregut in these mutant embryos form an excessive number of lamellipodia. Some of the mutant macrophages contain two nuclei.
Rac1V12.Scer\UAS expression causes Tv axons to stall before reaching the midline and fail to innervate the dorsal neurohemal organs.
After late stage 12 the tracheal primordia of Rac1V12.Scer\UAS; Scer\GAL4btl.PS embryos lose their branched morphology: cells budding from the tracheal primordia remain attached by thin stalks of cytoplasm for around 30 minutes before being expelled into the body cavity. This process is co-incident with a loss of polarity in these cells. By stage 15 the tracheal primordia fuse together to form one or two cell clusters on either side of the body cavity.
S2R+ cells expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Act5C.PKu show a dramatic increase in the level of cortical F-actin.
When Rac1V12.Scer\UAS is driven in the eye by Scer\GAL4GMR.PF, a mild rough eye phenotype and a complete loss of ommatidia is seen in the posterior region. When Rac1V12.Scer\UAS is driven by Scer\GAL4elav-C155, 29% of ISNb are arrested at the site of contact with ventral longitudinal muscle 13 before reaching their final target, muscle 12. No midline crossing longitudinal connectives is seen.
When Rac1V12.Scer\UAS is driven by Scer\GAL4repo in embryos, they display collapsed glial sheaths as well as PNS glial migration defects. The lateral line glia fail to connect across hemi-segments.
When Rac1V12.Scer\UAS is driven by Scer\GAL4ftz.ng, midline crossovers are seen in the pCC/MP2 pathway axons in 77% of embryos. An average of 2.4 crossovers are seen per embryo. When Rac1V12.Scer\UAS is driven by Scer\GAL4elav.PLu, no adults eclose.
Expression of Rac1V12.Scer\UAS, driven by Scer\GAL4332.3 results in failure to secrete cuticle in 41% of embryos. In embryos which do manage to secrete cuticle, 47% show puckering of the dorsal surface. In early stage 14 embryos Rac1V12.Scer\UAS expression, driven by Scer\GAL4332.3, results in contraction of the amnioserosa, with greatly constricted cells that occupy less than half of the dorsal hole at its posterior end. In wild-type embryos, only the end amnioserosa cells constrict but Rac1V12.Scer\UAS overexpression causes constriction of all cells. A similar effect is seen when Rac1V12.Scer\UAS expression is induced through heat shock by the Scer\GAL4hs.PB driver. In stage 15 embryos expressing Rac1V12.Scer\UAS driven by Scer\GAL4332.3 there is bunched closure of the epidermis around the amnioserosa causing the embryos to become bowed, with their heads and tails pulled in towards each other. This effect is likewise seen in embryos where Rac1V12.Scer\UAS expression is driven by Scer\GAL4hs.PB. Although overexpression of Rac1V12.Scer\UAS driven by Scer\GAL4c381 does not cause failure of cuticle formation, cuticles show puckers extending out from the dorsal surface. Such embryos fail to undergo germband retraction but are able to complete dorsal closure. As with expression driven by Scer\GAL4332.3, Scer\GAL4c381-driven expression of Rac1V12.Scer\UAS causes the same bunched closure of the epidermis and contraction of the amnioserosa.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4SG18.1 has no effect on the peripheral organisation of the olfactory neurons, but the neurons are disturbed within the olfactory lobe and the inter-antennal commissure is not formed.
Clones of cells expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Act5C.PP are not recovered in the nurse cell follicle cells. Clones of cells expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Act5C.PP in the posterior follicle cells but not in the main body portion result in posterior cells both in and adjacent to the clone delaminating and leaving the continuous follicle epithelium.
When Rac1V12.Scer\UAS is driven by Scer\GAL4slbo.2.6 border cell migration is completely blocked. When clones of Rac1V12.Scer\UAS are created in the follicle cells (driven by Scer\GAL4Act5C.PI) a dramatic accumulation of F-Actin in these cells is seen.
Embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4ptc-559.1 are completely disorganised and produce only random pieces of cuticle.
Scer\GAL4A307; Rac1V12.Scer\UAS flies at 25[o]C do not survive till adulthood. Adult progeny raised at 18[o]C exhibit gross GF abnormalities, with no neurite extensions.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4ey.PH results in an extreme reduction in the size of the eye disc.
Frequent defects in the projection pattern of VUM neurons are seen in stage 14 embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4sim.PS. At stage 16, a fused commissure phenotype is seen.
When Rac1V12.Scer\UAS is driven in postmitotic neurons by Scer\GAL460 it effects dendrite outgrowth at low penetrance.
Embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4ptc-559.1 or Scer\GAL4hs.PB (using heat shock) usually only produce small pieces of cuticle. The embryos show a dramatic bunching of the lateral epidermis around the amnioserosa. Rac1V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB suppresses the failure of dorsal closure caused by expression of Rac1N17.hs.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL448Y in the developing midgut does not result in accelerated migration of the endodermal midgut cells.
Scer\GAL4elav-C155-mediated expression causes arrest of the ISNb growth cone when it contacts with muscle 14.
Scer\GAL4how-24B-mediated expression causes myoblasts to distribute into groups at locations corresponding to ventral, lateral and dorsal muscle groups and the myoblasts generally fail to fuse. 10% myoblasts do fuse forming rudimentary myotubes, the remaining unfused cells have a more elongated morphology. Many prefusion complexes are present, electron dense membrane plaques are present and cells appear to elongate and align normally. However, only in a few cases does the plasma membrane vesiculate in any serious way, few membrane pores are observed. By stage 14 many myoblasts are dead, dying or cleared by macrophages.
When driven by a Scer\GAL4 line expressed under the influence of an elav promoter, the SNb motor neuron bundle is missing.
Scer\GAL4198Y-mediated expression does not causes border cell migration defects.
Embryos exhibit spontaneous and evoked muscle contraction with Scer\GAL4elav.PLu and Scer\GAL460, little muscle contraction with Scer\GAL41407 and no muscle contraction, abnormal gut and tracheae with Scer\GAL4how-24B (the segmentally repeated myoblast cells fail to fuse with each other). When in combination with Scer\GAL41407 one copy of Rac1L89.Scer\UAS causes some axonal loss between the lateral and dorsal clusters, two copies causes greater loss. One copy of Rac1Scer\UAS.cLa ameliorates this axonal loss. Scer\GAL4elav.PLu causes permanent arrest of the axons moving from the dorsal to lateral cluster.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Suppressed by
NOT suppressed by
Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
Rac1V12.UAS, Scer\GAL4hs.2sev has ommatidium phenotype, enhanceable by Frl[+]/FrlExK62
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference
Scer\GAL460/Rac1V12.UAS is an enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference
The intermediate-term olfactory memory defects resulting from the adulthood-only expression of Rac1V12.Scer\UAS, under the combined control of Scer\GAL4ey-OK107 and Gal80[ts], are enhanced by Rgk1Δ heterozygosity, are fully suppressed by the co-expression of Rgk1Scer\UAS.B.T:Avic\GFP, are partially suppressed by the co-expression of Rgk1ΔN.Scer\UAS.B.T:Avic\GFP, and are not suppressed by the co-expression of Rgk1ΔC.Scer\UAS.B.T:Avic\GFP.
Co-expression of scribKK106065 does not affect the memory performance of flies expressing Rac1V12.Scer\UAS under the control of Scer\GAL4GMR13F02 (in combination with a Gal80[ts] transgene to restrict expression to the adult stage).
Presence of FrlEx83/+ or FrlEx88/+ does not enhance eye phenotypes in flies with Rac1V12.Scer\UAS driven by Scer\GAL4hs.2sev; presence of FrlExK62/+ enhances ommatidial rotation defects. Expression of FrlDN.Scer\UAS driven by Scer\GAL4sev.EP enhances (likely additive) eye phenotypes (ommatidial rotation defects and R-cell loss) in flies with Rac1V12.Scer\UAS driven by Scer\GAL4hs.2sev.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4elav.Switch.PO (and feeding with RU486 to induce expression via the GeneSwitch system) significantly suppresses the reversal-learning defect observed in Fmr15-HA-1014/Fmr15-HA-1014 mutants.
Expression of Rac1V12.Scer\UAS via Scer\GAL4sns.PK partially rescues the msk4 embryonic muscle detachment phenotype.
Expression of Rac1V12.Scer\UAS suppresses the loss of F-actin rich protrusions seen in macrophages isolated from animals expressing SbfGD12081 under the control of Scer\GAL4Cg.PA.
Severely reduced eyes are produced in homozygous CRMPsupK1 animals also expressing Rac1V12.Scer\UAS under the control of Scer\GAL4sev.EP.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4twi.PU partially rescues mesodermal cell morphology in pbl2/pbl3 embryos: cellular protrusions are restored, but the defect in cell rounding is not rescued.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4sns.PK rescues myoblast fusion in homozygous mbcD11.2 embryos such that the somatic muscle pattern is almost wild type. Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4kirre-rP298 does not rescue myoblast fusion in homozygous mbcD11.2 embryos.
Expression of a constitutively active form of Rac1, Rac1V12.Scer\UAS under the control of Scer\GAL460, significantly increases the occurrence of ISNb bypass in Nl1N-ts1 embryos.
Expression of Mad1/Madk00237 fails to suppress the larval neuromuscular junction overgrowth and bouton number phenotypes seen when Rac1V12.Scer\UAS is expressed in motor neurons under the control of Scer\GAL4BG380. Expression of witA12/witHA3 fails to suppress the larval neuromuscular junction overgrowth and bouton number phenotypes seen when Rac1V12.Scer\UAS is expressed in motor neurons under the control of Scer\GAL4BG380. trioS137203/trio6A does not suppress the larval neuromuscular junction overgrowth and increase in bouton number seen when Rac1V12.Scer\UAS is expressed in motor neurons under the control of Scer\GAL4BG380.
Expression of Rac1V12.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 Rac1V12.Scer\UAS under the control of Scer\GAL4twi.2PE enhances the mesodermal migration defects seen in pbl5 homozygotes.
Heterozygous fra4 partially suppresses the incorrect midline crossing phenotype of ventral nerve cord axons in embryos overexpressing Rac1V12.Scer\UAS via Scer\GAL4ftz.ng. Co-expression of fraScer\UAS.cKa with Rac1V12.Scer\UAS under the control of Scer\GAL4ftz.ng results in a strong synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1V12.Scer\UAS-overexpression alone.
pucGS16811/+ significantly enhances the defects in left-right asymmetry of the anterior midgut which are seen in embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Gap1-NP3392. 20% of the double mutant embryos show inversion of the normal left-right asymmetry and 42% show no left-right asymmetry.
The salivary gland defects seen in embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4fkh.PH are partially suppressed by co-expression of shgScer\UAS.T:Avic\GFP-rs. Co-expression of shiK44A.Scer\UAS partially restores salivary gland integrity in embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4fkh.PH, but the glands are narrower and have fewer cells than wild type.
The combination of Sra-1EP3267 and Rac1V12.Scer\UAS driven by Scer\GAL4GMR.PF has a weaker eye phenotype than Rac1V12.Scer\UAS (driven by Scer\GAL4GMR.PF) alone. These phenotypes are enhanced by heterozygous Sra-1unspecified. The combination of Sra-1EP3267 and Rac1V12.Scer\UAS driven by Scer\GAL4elav-C155 has a ISNb stalling phenotype (only 17% exhibit the phenotype compared to 29%) than Rac1V12.Scer\UAS (driven by Scer\GAL4elav-C155) alone. These phenotypes are enhanced by heterozygous Sra-1unspecified (Stalling reaches 53%). In Rac1V12.Scer\UAS, Scer\GAL4elav-C155 embryos combined with heterozygous Sra-1unspecified, midline crossing of longitudinal connectives is seen.
The addition of Rac1V12.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 100% of embryos exhibit the phenotype. An average of 6.5 crossovers are seen per embryo. The addition of Rac1V12.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49 homozygous embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. % of embryos exhibit the phenotype. An average of crossovers are seen per embryo. The addition of chicsand-1 to Rac1V12.Scer\UAS suppresses the midline crossover phenotypes in the pCC/MP2 pathway axons. 57.3% of embryos exhibit the phenotype. An average of 1.5 crossovers are seen per embryo.
When Rac1V12.Scer\UAS is expressed by heat shock using the Scer\GAL4hs.PB driver in a crbS010409 homozygous mutant background, mutants no longer show contraction of the entire amnioserosa. These embryos show premature apical constriction of cells at the anterior end of the amnioserosa prior to the onset of dorsal closure in a manner similar to that seen crbScer\UAS.cWa overexpression driven by Scer\GAL4332.3.
Co-expression of RacGAP84CScer\UAS.cRa suppresses the phenotype caused by expression of Rac1V12.Scer\UAS under the control of Scer\GAL4ptc-559.1 so that 1/3 of embryos have only limited cuticle defects (in the anterior region).
The HemJ4-48 mutant phenotype is partially rescued by expression of Rac1V12.Scer\UAS under the control of Scer\GAL4sim.PS; the longitudinal connectives appear further apart and the commissures appear separated. VUM neurons are often seen projecting normally at the midline.
Xenogenetic Interactions
Statement
Reference
Expression of Rac1V12.Scer\UAS further enhances the dendrite defects seen in class IV da neurons expressing Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ppk.PG.
Co-expression of Ggal\MLCKct.Scer\UAS with Rac1V12.Scer\UAS under the control of Scer\GAL4ftz.ng results in a synergistic increase in the frequency of incorrect axon projections across the midline, compared with Rac1V12.Scer\UAS-overexpression alone.
Embryos co-expressing BacA\p35Scer\UAS.cHa and Rac1V12.Scer\UAS under the control of Scer\GAL4fkh.PH have abnormally shaped salivary glands that appear to consist of a disorganised cluster of cells, and a salivary gland lumen cannot be detected.
The addition of Rac1V12.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 95% of embryos exhibit the phenotype. An average of 4.2 crossovers are seen per embryo.
Complementation and Rescue Data
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Mutant
Wild-type
Stocks (2)
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Discoverer
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Synonyms and Secondary IDs (8)
Reported As
Symbol Synonym
Rac1V12.Scer\UAS
Rac1V12.UAS
Name Synonyms
Secondary FlyBase IDs
  • FBal0038996
References (83)