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General Information
Symbol
Dmel\Rac1N17.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0038994
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rac1N17, UAS-RacN17, UAS-RacN17, RacN17, UAS-Drac1N17, UAS-Drac1N17, UAS-rac1.N17, Rac1DN, UAS-Drac1(N17), UAS-Rac1N17
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 Rac1 (carries the amino acid replacement T17N) 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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

axon & dorsal cluster neuron, with Scer\GAL4ato.3.6

dendritic spine & lobular plate tangential neuron, with Scer\GAL4DB331

embryonic leading edge cell & actin filament, with Scer\GAL4en-e16E

rhabdomere & actin filament, with Scer\GAL4unspecified

rhabdomere & microvillus, with Scer\GAL4unspecified

Detailed Description
Statement
Reference

Third instar larvae expressing Rac1N17.UAS under the control of Scer\GAL4elav-C155 display supernumerary mature and satellite NMJ boutons. A significant increase in the number of synaptic boutons containing microtubule loops points towards an increase in microtubule stability.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4GMR13F02 (in combination with a Gal80[ts] transgene to restrict expression to the adult stage) results in enhanced memory after conditioning in an olfactory conditioning assay.

The mushroom body axons of flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4ey-OK107 display axonal growth defects in the lobe region.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 alters border cell cluster migration, with changes in local protrusion and retraction behaviour.

Scer\GAL4btl.PS-mediated expression of Rac1N17.Scer\UAS causes extension defects in the tracheal ganglionic branch.

Expression of Rac1N17.Scer\UAS specifically in adult glia (under the control of Scer\GAL4repo and Scer\GAL80ts.αTub84B) results in a potent suppression of axonal debris clearance.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4GMR.PU results in a rough eye phenotype.

The follicle cells of degenerating egg chambers from flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4GR1 show defects in the normal engulfment of dying germline cells. Unlike in wild type, the follicle cells fail to enlarge as nurse cell chromatin condenses and minimal uptake of nuclear fragments is seen. As egg chamber death progresses, the follicle cells die at the later stages. This phenotype is seen in both the presence and absence of starvation, however the follicle cells from starved flies usually do not die until later phases.

Class III ddaA neurons expressing Rac1N17.Scer\UAS under the control of Scer\GAL41003.3 show a significant decrease in the number of dendritic sensory filopodia compared to wild type. The average length of the filopodia is significantly decreased compared to wild type, while the total length of primary dendritic branches is not altered.

Larvae expressing Rac1N17.Scer\UAS under the control of Scer\GAL41003.3 show a reduced response to gentle touch compared to controls.

Flies with induced expression of Rac1N17.Scer\UAS for three days under the control of Scer\GAL4elav-C155 and Scer\GAL80ts.αTub84B show a remarkable tolerance to paraquat-induced oxidative stress, desiccation, starvation and high temperature. These flies survive for 50-100% longer than control flies in adverse conditions.

The body weight of flies expressing of Rac1N17.Scer\UAS for three days under the control of Scer\GAL4elav-C155 and Scer\GAL80ts.αTub84B is largely comparable to un-induced controls, although a marginal but statistically significant increase is found in males. The level of triglyceride, the primary storage form of lipid, is not altered either. The fecundity of female flies as determined by the number of eggs laid per fly per day is not compromised compared to that of controls.

Continuous expression of Rac1N17.Scer\UAS under the control of Scer\GAL4elav-C155 and Scer\GAL80ts.αTub84B (with flies kept at 30[o]C) does not confer any obvious beneficial or detrimental effects on life span.

Flies with induced expression of Rac1N17.Scer\UAS for three days under the control of Scer\GAL4Cha.7.4 and Scer\GAL80ts.αTub84B exhibit improved survival rates compared to controls when exposed to 20 mM paraquat and desiccation.

Flies with induced expression of Rac1N17.Scer\UAS for three days under the control of Scer\GAL4repo and Scer\GAL80ts.αTub84B do not exhibit improved survival rates compared to controls when exposed to 20 mM paraquat and desiccation.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL460 results in a low frequency of axonal 'stalling' phenotypes.

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 Rac1N17.Scer\UAS under the control of Scer\GAL4NP2432.

Expression of Rac1N17.Scer\UAS driven by Scer\GAL4slbo.2.6 results in the impairment of border cell migration during egg chamber development.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not block germ cell transepithelial migration or later germ cell migration.

Adult flies conditionally expressing Rac1N17.Scer\UAS under the control of Scer\GAL4elav.PU (using tub-Gal80[ts] to limit the expression to the adult stage) display significantly slower memory decay at later time-points but perform comparably to wild-type at early time-points shortly after the training stage in an aversive olfactory assay. The immediate (3 min) memory performance is unaffected regardless of the training intensity (electric shock intensity or number of pulses); the prolonged memory effect lasted less than four days, memory retention of adult flies on day 4 after 10 spaced training sessions is not significantly higher compared to controls. However, sensimotor responses of Rac1N17.Scer\UAS expressing flies to electric shock or odors used in the conditioning are comparable to controls.

Cold shock amnesia treatment applied 2 hr after training completely abolished the enhanced 3hr and 24hr memory performance of adult flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4elav.PU (using tub-Gal80[ts] to limit the expression to the adult stage) while treatment with cycloheximide had no effect on their long-term memory performance.

Adult flies conditionally expressing Rac1N17.Scer\UAS under the control of either Scer\GAL4ey-OK107 or Scer\GAL4238Y (using tub-Gal80[ts] to limit the expression to the adult stage) display enhanced 3 hr memory in an aversive olfactory assay compared to controls, this memory enhancement is not observed when any of the following drivers are used: Scer\GAL4Orco.PU, Scer\GAL4OK66, Scer\GAL4GH146, Scer\GAL4Feb170 or Scer\GAL4Alp4-c232. The memory enhancement is also not observed when Rac1N17.Scer\UAS is driven by Scer\GAL4ey-OK107 in the presence of Scer\GAL80Mef2.mb247 (expressed in the mushroom body). Of several subtype-specific mushroom body drivers tested, only expression under the Scer\GAL4D52H driver leads to 3hr memory enhancement, expression controlled by the others (Scer\GAL417d, Scer\GAL4c739, Scer\GAL4c305a, Scer\GAL41471, Scer\GAL4NP1131, Scer\GAL4Tab2-201Y, Scer\GAL4NP0065 and Scer\GAL4c320) had no effect.

Retroactive interference (training flies to acquire a novel odor-shock association) introduced at 1.5 hr after the initial learning has no effect on memory retention of the initial odor-shock association (but the acquisition of new learning is not impaired) in flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4elav.PU (using tub-Gal80[ts] to limit the expression to the adult stage), while in wild-type it leads to interference induced forgetting . The Rac1N17.Scer\UAS expressing adults perform significantly worse compared to wild-type in a reversal learning aversive olfactory assays (in which the odor-shock contingency is reversed in each training session and wild-type flies tend to avoid the odor paired with punishment most recently). This suggests that Rac1N17.Scer\UAS expressing flies have impeded forgetting and thus are less able to remove inappropriate old memories during reversal learning.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4DB331 does not alter the overall dendritic architecture in the lobular plate tangential cells; neither the position not branching patterns of primary and secondary order dendrites are affected. However, there is an increase in spine density and a change in spine morphology (the spines appear shorter and less well defined) compared to controls.

Scer\GAL4GMR.PU-mediated expression of Rac1N17.Scer\UAS results in a severe rough eye.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4GMR.PF results in a weak axonal hyperfasciculation phenotype in the lamina and medulla.

The salivary gland fails to migrate posteriorly and some cells remain at the ventral surface in embryos expressing Rac1N17.Scer\UAS under the control of Scer\GAL4fkh.PH.

Expression of Rac1N17.Scer\UAS under the control of cer\GAL4ato.3.6 results in a marked increase in the number of axons from dorsal cluster neurons crossing the optic chiasm (an average of only 19.8 axons crossing in contrast to the wild-type average of 11.7).

Expression of Rac1N17.Scer\UAS in myoblasts, driven by Scer\GAL41151, affects indirect flight muscles. There is a reduction in the mean number of dorsal longitudinal muscle (DLM) fibers (from 6 to ~4) and in DLM size (35% reduction in area). Additionally, the tergal depressor of trochanter (TDT) and the dorso-ventral muscles (DVMs) are almost completely absent. Expression of Rac1N17.Scer\UAS, under the control of Scer\GAL41151, does not affect the number of adult muscle precursors present at late embryonic stages. However, there is an approximately 43% reduction in the number of myoblast numbers in the wing discs of third instar larva. Experiments using Scer\GAL80ts.αTub84B show that Rac1N17.Scer\UAS needs to be expressed during larval stages to affect muscle development. Expression of Rac1N17.Scer\UAS, under the control of Scer\GAL41151, affects pupal myogenesis. DLM myoblast expansion and proliferation follows a different pattern in Scer\GAL41151/+; Rac1N17.Scer\UAS/+ mutants compared to controls: in the mutants there is no significant increase of proliferation at 12-16 hours APF and there is a sharp decline in expanse by 20 hours APF. At 16 hours APF, Scer\GAL41151/+; Rac1N17.Scer\UAS/+ myoblasts undergo less fusion than controls. Fiber formation is delayed compared to controls, and by 24 hours APF, the majority of Scer\GAL41151/+; Rac1N17.Scer\UAS/+ mutants have only 3 DLM fibers, instead of the wild-type number of 6. Pupal myogenesis is severely affected in the DVMs of Scer\GAL41151/+; Rac1N17.Scer\UAS/+ mutants. Myoblast proliferation fails to increase at 12-16 hours APF and there is a sharp decline at 20 hours APF. At 16 hours APF, Scer\GAL41151/+; Rac1N17.Scer\UAS/+ DVM myoblasts are disorganized and are not aligned along the long axis of the founder cells, as occurs in wild type. At 20-24 hours APF, control myoblasts become compact and rounded, while Scer\GAL41151/+; Rac1N17.Scer\UAS/+ DVM myoblasts fail to assume this shape. Myoblast segregation and fusion does not occur in the mutants. By 20 hours APF, when DVM fiber formation is complete in controls, myoblasts of Scer\GAL41151/+; Rac1N17.Scer\UAS/+ mutants remain unpatterned.

When Rac1N17.Scer\UAS is driven by Scer\GAL4elav.PLu, embryos display mild midline axon outgrowth defects, with small breaks in the outermost longitudinal pathways, with rare axons ectopically crossing the midline.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4arm.PS does not affect ventral patterning in the embryo, but causes a dorsal hole phenotype.

Expression of Rac1N17.Scer\UAS in border cells, driven by Scer\GAL4slbo.2.6, inhibits the migration of border cell clusters to the oocyte. However, the apical cap of these egg chambers forms and is shed normally.

Expression of Rac1N17.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 Rac1N17.Scer\UAS embryos than in wild-type, indicating that the VNC fails to condense correctly in Rac1N17.Scer\UAS mutants. Expression of Rac1N17.Scer\UAS in the lateral glia, driven by Scer\GAL4158, results in inhibition of VNC condensation in embryos but does not affect the differentiation or survival of the lateral glial cells. Expression of Rac1N17.Scer\UAS throughout the CNS, driven by Scer\GAL4elav-C155, does not affect the condensation of the VNC in embryos.

Expression of Rac1N17.Scer\UAS in the aCC/RP2 axons (under the control of Scer\GAL4eve.RN2), results in stalling in 15.2% of hemisegments. Stalled aCC/RP2 axons cause a co-arrest of the complete intersegmental motor nerve in 90% of cases.

Expression of Rac1N17.Scer\UAS, under the control of Scer\GAL4slbo.2.6, inhibits border cell migration.

Developmental dispersal of hemocytes is abnormal in embryos expressing Rac1N17.Scer\UAS under the simultaneous control of both Scer\GAL4Pxn.PS and Scer\GAL4crq.PA.

One hour after laser-induced wounding, approximately half the number of hemocytes are recruited to the wound in embryos expressing Rac1N17.Scer\UAS under the simultaneous control of both Scer\GAL4Pxn.PS and Scer\GAL4crq.PA compared to wild type embryos. Hemocytes that are recruited in the mutant embryos have significantly reduced lamellar protrusions.

Expression of Rac1N17.Scer\UAS in segmental stripes of the embryonic epithelium, driven by Scer\GAL4en-e16E, inhibits the production of actin protrusions and the actin cable within epithelial cells. These embryos are able to complete dorsal closure but the Rac1N17.Scer\UAS-expressing cells fail to fuse properly, which results in the presence of small holes in the midline. These embryos also show segmental mismatching along the midline.

Expression of Rac1N17.Scer\UAS in the muscle, under the regulation of Scer\GAL4Mhc.PW has no effect on synapse development.

Rac1N17.Scer\UAS; Scer\GAL41151 pupae have severely reduced myoblast fusion, the effect being most dramatic in the lateral muscles of the abdomen and, to a lesser extent, in the thoracic muscles. The lateral muscles of the abdomen in these pupae don't fuse and the resulting unfused myoblasts cluster around founder myoblasts, but do not differentiate further. Each unfused founder cell elongates and differentiates into a thin myotube eventually eventually developing into a mononucleate fibre. By contrast, some fusion does occur in the developing dorso-ventral indirect flight muscles. The putative founders myoblasts of these muscles are present in the pupal thorax in a wild-type pattern. These founders initiate fibre formation, but to a lesser extent than normal, leading to the formation of fibres with fewer nuclei than wild-type fibres of the same stage. The resulting muscles are abnormally thin, but form at the correct position and with the correct number of fibres.

When Rac1N17.Scer\UAS is driven by Scer\GAL4477, no detectable phenotype is seen in dendrites.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 results in defects in border follicle cell migration in more than 95% of stage 10 egg chambers. Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 does not results in apoptotic cells in stage 10 egg chambers. Expression of Rac1N17.Scer\UAS under the control of Scer\GAL469B or Scer\GAL4pnr-MD237 results in a failure of dorsal closure and lethality. Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4how-24B results in dramatic defects in myoblast fusion.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4gcm-rA87.P blocks macrophage migration in embryos; only a few macrophages move anteriorly and posteriorly for short distances.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4Cg25C-A109.1F2.P causes macrophages to clump in various areas of the embryo (such as the head region, around the pharynx, midgut and hindgut and laterally along the ventral cord). This defect is seen at stage 16, but becomes more pronounced during stage 17. The macrophages are abnormal in shape in the mutant embryos, appearing rounder than normal due to a block in the formation of cellular protrusions.

Macrophages expressing Rac1N17.Scer\UAS under the control of Scer\GAL4unspecified show wild-type levels of cortical F-actin. The macrophages have few or no cytoplasmic extensions in the mutant embryos.

Flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4GMR.PU have rough eyes with a loss of rhabdomeres, abnormal photoreceptor cells, vacuolated material in the retina and polarity defects.

When expression is driven by Scer\GAL4He.PZ, hemocyte proliferation is unaffected, lamellocytes are abnormal and replaced by multinucleate cells that do not express lamellocyte markers and crystal cells are decreased.

Rac1N17.Scer\UAS; Scer\GAL4btl.PS embryos have tracheal defects including truncated and/or zig-zagged dorsal trunk, misguided dorsal branches and a lack of terminal branches. The cell rearrangements occurring during extension of the dorsal branches towards the dorsal midline are greatly inhibited in these embryos: migration of cells to form the dorsal branch begins, but the number of cells contributed is less than in wild-type, and the resulting dorsal branches are shorter, occasionally failing to form at all.

When Rac1N17.Scer\UAS is overexpressed under the control of Scer\GAL4elav.PLu, mutants do not exhibit longitudinal axon ectopic midline crossing defects.

Although Rac1N17.Scer\UAS; Scer\GAL4elav.PLu embryos have occasional defects in the segmental nerve (SN)b and SNa motoneurons, they always extend their axons out of the CNS (as part of the abdominal posterior fascicle). In some cases (16%), the lateral branch of SNa motor axon actually extends beyond its target muscles.

Rac1N17.Scer\UAS driven by Scer\GAL4GMR.PF gives a rough eye phenotype.

When Rac1N17.Scer\UAS is driven by Scer\GAL4repo, mutant embryos have mildly disrupted glial wrapping profiles with occasional small gaps in the nerve sheath. Sensory neurons also show defasciculation.

When Rac1N17.Scer\UAS is driven by Scer\GAL4ftz.ng, no midline crossovers are seen in the pCC/MP2 pathway axons. When Rac1N17.Scer\UAS is driven by Scer\GAL4elav.PLu, no adults eclose.

Expression of Rac1N17.Scer\UAS, driven by Scer\GAL4332.3, causes a failure to secrete cuticle in 61% of embryos and holes in the dorsal surface of 8% of embryos that do manage cuticle secretion. Expression of Rac1N17.Scer\UAS, driven by Scer\GAL4332.3, results in impairment of amnioserosa morphogenesis and migration of the epidermis. The amnioserosa of these mutants remains elliptical at an age where the same tissue is narrowing in wild type. This lack of morphological change appears to impede the movement of the epidermis resulting in a dorsal hole which is larger than in wild type. Within a single mutant embryo there may be patches of cells that change shape correctly and patches that do not. The progression of the epidermis is impeded more around patches of cells that have failed to change shape. Overexpression of Rac1N17.Scer\UAS driven by Scer\GAL4c381 does not cause failure of cuticle formation. However, embryos do fail to complete dorsal closure and have a large dorsal hole in the cuticle extending from the middle of the dorsal surface to the rear of the embryo. Additionally, the epidermis fails to migrate over the amnioserosa.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4btl.PS does not affect lumen formation in the tracheal system although these embryos do show some defects in tracheal branch migration.

77.6% of ommatidia in mutant somatic clones (driven by Scer\GAL4hs.2sev) in the eye are normal. 18.1% have rotated ommatidia, 0.5% have chirality defects, 0.7% are achiral (3.1% unscorable).

Co-expression of Rac1N17.Scer\UAS has little or no effect on the gain of function axon guidance defects caused by expression of Gef64CEP3035 under the control of Scer\GAL4elav.PLu.

Clones of cells expressing Rac1N17.Scer\UAS under the control of Scer\GAL4Act5C.PP in the nurse cell follicle cells results in aberrant morphology.

When Rac1N17.Scer\UAS is driven by Scer\GAL4elav.PLu dramatic effects are seen on axon guidance. The intersegmental nerve b (ISNb) fails to branch off and enter the ventral muscles and instead follows the ISN distally toward dorsal muscles. The SNa motor axons also sometimes abnormally project to lateral muscle targets, bypassing their normal targets.

Embryos expressing Rac1N17.Scer\UAS under the control of Scer\GAL4ptc-559.1 have a dorsal hole.

Eggs derived from females expressing Rac1N17.Scer\UAS under the control of Scer\GAL4T155 have short dorsal appendages. Eggs derived from females expressing Rac1N17.Scer\UAS under the control of Scer\GAL4CY2 show a failure of the dorsal appendages to elongate.

Approximately 70% of axons expressing Rac1N17.Scer\UAS under the control of Scer\GAL4A307 exhibit morphological abnormalities such as excess branching in the target region. The axons often send ectopic projections across the midline into the contralateral side of the ganglion in T2 or extra processes down into T3, a phenotype never seen in controls. In some cases one GF splits and makes bilateral bends while its partner grows on into T3 without making any bend. Often the axons split several times sending a number of projections to inappropriate parts of the ganglion. In addition to these extra processes the lateral bends, along which the synapse with the TTMn can be formed, are always seen in T2.

The function of the GF-TTMn synapse in Scer\GAL4A307; Rac1N17.Scer\UAS flies in both the response latency and the percentage following at 250Hz are normal.

Dendritic defects are seen in about 25% of Scer\GAL4A307; Rac1N17.Scer\UAS GFs. The dendritic field always contains its distinct domains, but the large dendrites have a brush-like appearance with many small processes emanating from the larger ones.

Approximately 81% of Scer\GAL4A307; Rac1Scer\UAS.cLa flies exhibit a bendless GF phenotype, while 64% of Scer\GAL4A307; Rac1Scer\UAS.cLa GFs are bendless. The remainder exhibit wild-type bends or large abnormally shaped processes in the target region.

When expression is driven by Scer\GAL4elav-C155, ISNb shows a bypass phenotype. The CNS shows similar breaks in longitudinal connectives to those of trio loss of function mutants.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4ey.PH results in uncoordinated differentiation in the eye disc.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4unspecified during rhabdomere morphogenesis results in reduced, disorganised rhabdomeres. Fewer microvilli than normal are seen in cross section and a well-defined rhabdomere base is not formed; apposed sheets of membrane are involuted into the photoreceptor cytoplasm. The actin cytoskeleton appears diffuse and disordered.

Rac1N17.Scer\UAS when driven by Scer\GAL4hs.2sev leads to planar polarity, defects in the eye. This phenotype is enhanced by the addition of Df(3L)Ar14-8, which removes the Rac1 gene. Although it is mostly ommatidial rotation that is randomised in Scer\GAL4hs.2sev, Rac1N17.Scer\UAS mutants the enhancement of the phenotype by Df(3L)Ar14-8 increases the number of symmetrical, achiral ommatidia. These phenotypes appear early in development, suggesting they are primary defects.

When expression is driven by Scer\GAL4sd-SG29.1 wing size is reduced.

Embryos expressing Rac1N17.Scer\UAS under the control of Scer\GAL4ptc-559.1 or Scer\GAL4hs.PB (using heat shock) have dorsal holes ranging in size from a small 'scab' to a wide open dorsal surface.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL448Y in the developing midgut causes a delay in migration of the endodermal midgut cells.

Expression of Rac1N17.Scer\UAS by Scer\GAL4prd.RG1 has no effect on cytokinesis or mitosis.

Scer\GAL4twi.PG-mediated expression causes severe cuticle defects.

Scer\GAL4elav-C155-mediated expression causes ISNb axons to extend past the ventral longitudinal muscles. ISNb axons may also form a distinct fascicle that follows the ISN beyond ventral muscles. Phenotype of segments showing any evidence of ISNb bypass or the full bypass phenotype is more severe with Scer\GAL41407 or Scer\GAL4elav.PLu-mediated expression. Scer\GAL4elav-C155-mediated expression causes the dorsal projection of SNa axons to extend beyond the distal edge of muscle 4 or the axons extend beyond the target site to make ectopic contacts onto dorsal muscles, sensory sheath cells or ISN axons. Phenotype is more severe with Scer\GAL41407 or Scer\GAL4elav.PLu-mediated expression. Scer\GAL4elav-C155-mediated expression causes defects in the morphology of the CNS pathways. Coexpression of Rac1Scer\UAS.cLa under the same Scer\GAL4 driver yields near normal morphology of the CNS pathways, some abnormalities can be seen in occasional segments.

Embryos exhibit a dorsal open phenotype.

Causes duplications and triplications of wing hairs when expressed using Scer\GAL4ptc-559.1. The duplicated or triplicated hairs are morphologically indistinguishable from wild-type. Actin distribution in Rac1N17.Scer\UAS expressing cells is abnormal at 30-35 hours after puparium formation, and microtubules appear disorganised 30-32 hours after puparium formation.

Scer\GAL4198Y- or Scer\GAL4306-mediated expression causes no or little border cell migration in 80% stage 10 egg chambers. 19 to 22% of laid eggs hatch. Scer\GAL4458-mediated expression causes arrested migration in 10% of stage 10 egg chambers. Removing Rac1 activity during migration (using Scer\GAL4hs.PB) seems to halt all activity.

Wing discs expressing Rac1N17.Scer\UAS using Scer\GAL4ptc-559.1 often contain dead cells that are extruded from the basal side of the epithelium. Adherens junction actin is disrupted in cells expressing Rac1N17.Scer\UAS. Wings derived from discs in which Rac1N17.Scer\UAS is expressed using Scer\GAL4ptc-559.1 are of normal length but narrow, with the reduction in wing area restricted to the anterior compartment. Wing hairs are often duplicated or triplicated, the penetrance of this phenotype decreasing at the wing margin.

Semi-embryonic lethal with Scer\GAL41407 and Scer\GAL4elav.PLu and viable with Scer\GAL460. Embryos with Scer\GAL4how-24B have weak muscle contractions.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
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Reference
NOT Enhanced by
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Suppressed by
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NOT suppressed by
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Rac1N17.UAS, Scer\GAL4sev.EP has visible phenotype, non-suppressible by CRMPsupK1

Enhancer of
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NOT Enhancer of
Suppressor of
NOT Suppressor of
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Other
Phenotype Manifest In
Enhanced by
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NOT Enhanced by
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Rac1N17.UAS, Scer\GAL4sev.EP has eye phenotype, non-enhanceable by CRMPsupK1

Rac1N17.UAS, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-enhanceable by dsh1

Rac1N17.UAS, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-enhanceable by btlUAS.cDa, Scer\GAL4ato.3.6

Suppressed by
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Reference

Rac1N17.UAS, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, suppressible by bskDN.UAS, Scer\GAL4ato.3.6

NOT suppressed by
Statement
Reference

Rac1N17.UAS, Scer\GAL4sev.EP has eye phenotype, non-suppressible by CRMPsupK1

Rac1N17.UAS, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-suppressible by dsh1

Rac1N17.UAS, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-suppressible by btlUAS.cDa, Scer\GAL4ato.3.6

Enhancer of
NOT Enhancer of
Statement
Reference

Rac1N17.UAS, Scer\GAL4ato.3.6 is a non-enhancer of axon & dorsal cluster neuron phenotype of Scer\GAL4ato.3.6, bskDN.UAS

Rac1N17.UAS, Scer\GAL4477 is a non-enhancer of multidendritic neuron & dendrite | supernumerary phenotype of Scer\GAL4477, trcK122A.UAS.L.Tag:FLAG/trcK122A.Scer\UAS.T:Zzzz\FLAG

Rac1N17.UAS, Scer\GAL4477 is a non-enhancer of multidendritic neuron & dendrite phenotype of Scer\GAL4477, trcK122A.UAS.L.Tag:FLAG/trcK122A.Scer\UAS.T:Zzzz\FLAG

Suppressor of
NOT Suppressor of
Statement
Reference

Rac1N17.UAS, Scer\GAL4ato.3.6 is a non-suppressor of axon & dorsal cluster neuron phenotype of Scer\GAL4ato.3.6, bskDN.UAS

Rac1N17.UAS, Scer\GAL4477 is a non-suppressor of multidendritic neuron & dendrite | supernumerary phenotype of Scer\GAL4477, trcK122A.UAS.L.Tag:FLAG/trcK122A.Scer\UAS.T:Zzzz\FLAG

Rac1N17.UAS, Scer\GAL4477 is a non-suppressor of multidendritic neuron & dendrite phenotype of Scer\GAL4477, trcK122A.UAS.L.Tag:FLAG/trcK122A.Scer\UAS.T:Zzzz\FLAG

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Genetic Interactions
Statement
Reference

Expressing Rac1N17.UAS under the control of Scer\GAL4elav-C155 in a witA12 background results in significantly fewer satellite boutons, but a similar number of mature synaptic boutons as controls at the NMJ of third instar larvae. The number of both bouton types is significantly reduced when expression is driven in a witA12/witB11 background.

Co-expression of Dop1R2Scer\UAS.cCSa does not affect the memory performance of flies expressing Rac1N17.Scer\UAS under the control of Scer\GAL4GMR13F02 (in combination with a Gal80[ts] transgene to restrict expression to the adult stage).

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4elav.Switch.PO (and feeding with RU486 to induce expression via the GeneSwitch system) fails to suppress the reversal-learning defect observed in Fmr15-HA-1014/Fmr15-HA-1014 mutants.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4332.3 fails to suppress the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background.

Flies expressing Rac1N17.Scer\UAS, PvrDN.Scer\UAS and EgfrDN.Scer\UAS exhibit a change in border cell migration, with changes in local protrusion and retraction behaviour that are different to those found in Rac1N17.Scer\UAS single mutants.

Flies expressing Rac1N17.Scer\UAS and PvrDN.Scer\UAS exhibit a change in border cell migration, with changes in local protrusion and retraction behaviour that are different to those found in Rac1N17.Scer\UAS single mutants.

Flies expressing Rac1N17.Scer\UAS and EgfrDN.Scer\UAS exhibit a change in border cell migration, with changes in local protrusion and retraction behaviour that are different to those found in Rac1N17.Scer\UAS single mutants.

Expression of Rac1N17.Scer\UAS specifically in adult glia (under the control of Scer\GAL4repo and Scer\GAL80ts.αTub84B) in a SosJC2/+ background, results in a 50% suppression of axon debris clearance, compared to wild-type.

Co-expression of Rac1N17.Scer\UAS fails to suppress the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2RE.Scer\UAS and Ras85DG12V.Scer\UAS under the control of Scer\GAL4tub.PU, and also fails to suppress the developmental delay shown by larvae containing these clones.

Animals expressing dominant-negative Rac1N17.Scer\UAS under the control of Scer\GAL4sev.EP display no discernible differences in the presence or absence of homozygous CRMPsupK1.

Overexpression of Rac1N17.Scer\UAS under the control of Scer\GAL415J2 suppresses the early longitudinal axon phenotype of Nl1N-ts1.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL460, significantly increases the occurrence of ISNb bypass in Nl1N-ts1 embryos.

Co-expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP with Rac1N17.Scer\UAS driven by Scer\GAL4slbo.2.6 enhances the border follicle cell migration phenotype associated with Rac1N17.Scer\UAS expression.

Co-expression of Rac1N17.Scer\UAS and Dcp-1Scer\UAS.cKa (insertion line P{UAS-Dcp-1.K}19-2) under the control of Scer\GAL4GMR.PF is lethal.

Expression of Rac1N17.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.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4NP2225 does not suppress 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.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4rut-1047 (using tub-Gal80[ts] to limit the expression to the adult stage) in rut1047 hemizygote adult males does not affect the acquisition defect characteristic for rut1047 mutants but it significantly improves their 3 hr memory performance compared to controls.

Expression of Rac1N17.Scer\UAS under the control of Scer\GAL4twi.2PE enhances the mesodermal migration defects seen in pbl5 homozygotes.

The Scer\GAL4GMR.PU, Rac1N17.Scer\UAS rough eye phenotype is suppressed by co-expression of Ced-12Scer\UAS.cGa and mbcScer\UAS.cBa.

The increased bouton number at the neuromuscular junction that is seen in Vps35EY14200/Df(2R)ED3952 larvae is suppressed by expression of Rac1N17.Scer\UAS under the control of either Scer\GAL4elav.PLu or Scer\GAL4C57.

The axonal hyperfasciculation phenotype in the lamina and medulla caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL4GMR.PF is enhanced by bure10/+.

Coexpression of bskDN.Scer\UAS and Rac1N17.Scer\UAS under the control of Scer\GAL4ato.3.6 results in the few dorsal cluster neuron axons crossing the optic chiasma, which is the same phenotype seen as single bskDN.Scer\UAS expression and is opposite to that seen when only Rac1N17.Scer\UAS is expressed.

Coexpression of btlScer\UAS.cDa and Rac1N17.Scer\UAS, under the control of Scer\GAL4ato.3.6, results in the dominance of the Rac1N17.Scer\UAS phenotype, with a large increase in the number of dorsal cluster neuron axons that cross the optic chiasm.

Coexpression of btlDN.Scer\UAS and Rac1N17.Scer\UAS, under the control of Scer\GAL4ato.3.6, results in all dorsal cluster neuron axons crossing the optic chiasm, instead of the majority retracting and branching within the lobula.

Expression of Rac1N17.Scer\UAS, under the control of Scer\GAL4ato.3.6, in a dsh1 background results in a dorsal neuron cluster phenotype similar to when Rac1N17.Scer\UAS is expressed in a wild-type background, which is opposite to that seen in dsh1 mutants.

When RhoGAP93BScer\UAS.cHa is added to RhoGAP93BScer\UAS.cHa, Scer\GAL4elav.PLu embryos, multiple axons exhibit ectopic crossing of the midline. On the other hand Cdc42N17.Scer\UAS does not enhance this phenotype.

When RhoGAP93BScer\UAS.cHa is added to Rac1N17.Scer\UAS, Scer\GAL4elav.PLu embryos, multiple axons exhibit ectopic crossing of the midline. On the other hand Cdc42N17.Scer\UAS does not enhance this phenotype.

Expression of osScer\UAS.cCa, hopTum.Scer\UAS or Stat92EScer\UAS.cPa suppress the border cell migration defect caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6. However, expression of awdScer\UAS.cDa does not suppress this phenotype.

Co-expression of Cdc42N17.Scer\UAS and Rac1N17.Scer\UAS in the muscle, under the regulation of Scer\GAL4Mhc.PW has no effect on gross synapse development.

The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by coexpression of trioScer\UAS.cBa, Act5CEP1604, thEP3308, thEP3279, thScer\UAS.T:Ivir\HA1 or Iap2Scer\UAS.cWa. The penetrance of the embryonic lethal phenotype caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL469B or Scer\GAL4pnr-MD237 is reduced by coexpression of thScer\UAS.T:Ivir\HA1. The embryonic cuticle phenotype (dorsal hole) caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL469B or Scer\GAL4pnr-MD237 is rescued by coexpression of thScer\UAS.T:Ivir\HA1. The dramatic defects in myoblast fusion caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL4how-24B are not rescued by coexpression of thScer\UAS.T:Ivir\HA1. The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by coexpression of chicScer\UAS.cCa. The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by coexpression of NcΔN.C-A.Scer\UAS or NcCARD.Scer\UAS. The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by ArkCD4/+, ArkCD8/+, ArkCD4/ArkCD4, ArkCD8/ArkCD8 or ArkCD4/ArkCD8. The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is not suppressed by coexpression of slboScer\UAS.cLa.

The combination of heterozygous sli2 and pan-neural overexpression of Rac1N17.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) leads to longitudinal axon ectopic midline crossing defects. An average of 8.3 defects are seen per animal, and an average of 75% of segments have defects. If expression of Rac1N17.Scer\UAS is driven by Scer\GAL4ftz.ng 4 defects are seen per animal, and an average of 36% of segments have defects. Co-expression of PakScer\UAS.T:Myr1 partially suppresses longitudinal axon ectopic midline crossing defects seen in sli2/+, Rac1N17.Scer\UAS ; Scer\GAL4elav.PLu animals. An average of 5 defects are seen per animal, and an average of 45% of segments have defects.

The addition of Rac1N17.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos has no effect on the midline crossover phenotype seen in the pCC/MP2 pathway axons. The addition of Rac1N17.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49 homozygous embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 91% of embryos exhibit the phenotype. An average of 8.0 crossovers are seen per embryo. The addition of chicsand-1 to Rac1N17.Scer\UAS has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons.

Embryos that express both crbScer\UAS.cWa and Rac1N17.Scer\UAS driven by Scer\GAL4332.3 show the premature apical cell constriction phenotype in the amnioserosa that is seen when crbScer\UAS.cWa expression alone is driven by Scer\GAL4332.3.

The addition of plexBScer\UAS.cHa to Rac1N17.Scer\UAS, Scer\GAL4elav.PLu flies enhances the ISNb bypass phenotype seen in these flies. The addition of plexBScer\UAS.cHa to Rac1N17.Scer\UAS, Scer\GAL4elav.PLu flies has no effect on the ISNb bypass phenotype seen in these flies. The addition of plexBScer\UAS.cHa to Rac1N17.Scer\UAS, Scer\GAL4elav.PLu flies significantly suppresses the ISNb bypass phenotype seen in these flies.

The addition of Rho1k07903 to Rac1N17.Scer\UAS,Scer\GAL4hs.2sev flies significantly enhances the eye phenotype. There is an increase in the number of achiral ommatidia.

tkvTAJ3 partially rescues the dorsal closure defect caused by expression of Rac1N17.Scer\UAS under the control of Scer\GAL4hs.PB.

Scer\GAL4elav-C155-mediated expression causes synergy of the Lar5.5, Lar13.2 and Larbypass full ISNb bypass phenotype. Synergistic interaction is not seen in beat-Ia2/beat-Ia3 embryos.

The Rac1N17.Scer\UAS dorsal open phenotype can be significantly rescued by heat induced expression of JraAsp.hs.sev.

Xenogenetic Interactions
Statement
Reference

Border cell clusters expressing Rac1N17.Scer\UAS and Hsap\RAC1PA.Q61L.Scer\UAS.T:Disc\RFP-mCherry,T:Zzzz\PT1 under the control of Scer\GAL4slbo.2.6 in which Hsap\RAC1PA.Q61L.Scer\UAS.T:Disc\RFP-mCherry,T:Zzzz\PT1 has been activated by illumination in one cell do not show forward migration. However, photoactivation of Hsap\RAC1PA.Q61L.Scer\UAS.T:Disc\RFP-mCherry,T:Zzzz\PT1 in approximately half of the cluster results in slow forward movement.

The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is not suppressed by coexpression of Mmus\Cd8aScer\UAS.T:Avic\GFP. The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is not significantly suppressed by coexpression of BacA\p35Scer\UAS.cHa.

The addition of Rac1N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.0% of embryos exhibit the phenotype. An average of 1.o crossovers are seen per embryo.

Complementation and Rescue Data
Comments

The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by coexpression of Rac1Scer\UAS.cLa.

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  • FBal0038993
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