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General Information
Symbol
Dmel\Rac1J11
Species
D. melanogaster
Name
FlyBase ID
FBal0135835
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G1302168A

Amino acid change:

G60E | Rac1-PA; G60E | Rac1-PB

Reported amino acid change:

G?E

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: G60E.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Bouton numbers are unaffected at the NMJ of Rac1J11/+ third instar larvae.

Rac1J11 mutant larvae exhibit strong ECM detachment and epithelial enclosure of dendrites in class IV dendritic arborizing neurons.

Homozygous larvae show a strongly reduced rate of encapsulation (11%) of eggs of the avirulent wasp strain L. boulardi G486 compared to the rate seen in wild-type larvae.

65% of heterozygotes have normal alpha/beta mushroom body lobes and 35% have branching defects in the lobes.

Heterozygous and Rac1J11/Rac1J10 flies show normal resistance to infection with P.aeruginosa by septic injury.

The salivary gland cells invaginate in Rac1J11 mutant embryos, but the gland does not complete its posterior migration, but instead is abnormally shaped and appears attached to the ventral surface.

In contrast to wild-type animals, where only 38% of dorsal cluster neuron axons innervate the medulla, 87% of axons from Rac1J11 neuron clones innervate this region.

An ectopic collateral branch is observed on the small LNv projections in 17% of Rac1J11/+ adult brains. The posterior tract of the LNv neurons shows a defasciculation phenotype in 33% of brains.

46% of homozygous males are sterile in individual crosses with wild-type females, although the testes appear normal and the seminal vesicle is full of motile sperm.

No gross defects are seen in dendritic branching patterns are seen in later embryogenesis stages. however, when single cell mutant clones are made during larval stages, dendritic arborising neurons (DA neurons) exhibit fewer dendritic branches than wild-type. ddaC neurons exhibit a 23% reduction in the number of dendritic branches.

Homozygous mutant embryos show lack of peripheral glial coverage of lateral axon tracts and abnormal glial profiles are seen in the ventral region. The motor neuron projections and the lateral chordotonal sensory neurons are sometimes seen to be stalled.

Heterozygous adults show significant defects in branching of the mushroom body axons and some guidance defects in the mushroom body axons. Homozygotes show mainly guidance defects in the mushroom body axons. In mosaic animals, 21% of neuroblast clones show defective guidance.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference

Rac1J11/Rac1[+], Scer\GAL4GMR.PFa, egrUAS.cMa has visible | adult stage phenotype, non-enhanceable by Rac2Δ/Rac2[+]

Suppressed by
Statement
Reference

MtlΔ, Rac1J11, Rac2Δ has lethal | embryonic stage phenotype, suppressible | partially by hepCA.UAS/Scer\GAL4[-]

Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference

Rac1J11/Rac1[+] is a non-suppressor of visible phenotype of HIV-1\VpuUAS.cLa, Scer\GAL4dpp.blk1

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of HIV-1\VpuUAS.cLa, Scer\GAL4dpp.blk1

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

Other
Statement
Reference

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+], sickΔ, tsr[+]/tsrN96A has neuroanatomy defective phenotype

MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+] has neuroanatomy defective phenotype

Phenotype Manifest In
Enhanced by
Statement
Reference

DAAMEx68, Rac1J11 has neuropil phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11 has fascicle phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11 has connective phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11 has embryo phenotype, enhanceable by Rac2Δ

DAAMEx68, Rac1J11, Rac2Δ has neuropil phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has fascicle phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has connective phenotype, enhanceable by MtlΔ

DAAMEx68, Rac1J11, Rac2Δ has embryo phenotype, enhanceable by MtlΔ

Rac1J11 has ventral adult lateral neuron & commissure phenotype, enhanceable by Fmr1Δ113M/Fmr1[+]

Rac1J11 has LNv neuron phenotype, enhanceable by Fmr1Δ113M/Fmr1[+]

Rac1J11 has ventral adult lateral neuron & commissure phenotype, enhanceable by Dp(2;2)C619/+

Rac1J11 has LNv neuron phenotype, enhanceable by Dp(2;2)C619/+

Rac1J11, Rac2Δ/Rac2[+] has dorsal group branch precursor phenotype, enhanceable by bnl[+]/bnl00857

Rac1J11, Rac2Δ/Rac2[+] has tracheal branch primordium phenotype, enhanceable by bnl[+]/bnl00857

Rac1J11, Rac2Δ/Rac2[+] has dorsal trunk primordium phenotype, enhanceable by bnl[+]/bnl00857

Rac1J11, Rac2Δ/Rac2[+] has dorsal group branch precursor phenotype, enhanceable by btl[+]/btlΔOh10

Rac1J11, Rac2Δ/Rac2[+] has tracheal branch primordium phenotype, enhanceable by btl[+]/btlΔOh10

Rac1J11, Rac2Δ/Rac2[+] has dorsal trunk primordium phenotype, enhanceable by btl[+]/btlΔOh10

Rac1J11, Rac2Δ/Rac2[+] has dorsal group branch precursor phenotype, enhanceable by stumps09904b/stumps[+]

Rac1J11, Rac2Δ/Rac2[+] has tracheal branch primordium phenotype, enhanceable by stumps09904b/stumps[+]

Rac1J11, Rac2Δ/Rac2[+] has dorsal trunk primordium phenotype, enhanceable by stumps09904b/stumps[+]

NOT Enhanced by
Statement
Reference

Rac1J11/Rac1[+], Scer\GAL4GMR.PFa, egrUAS.cMa has eye phenotype, non-enhanceable by Rac2Δ/Rac2[+]

Suppressed by
Enhancer of
Statement
Reference

Rac1J11/Rac1[+] is an enhancer of mushroom body alpha-lobe phenotype of DAAMEx1

Rac1J11/Rac1[+] is an enhancer of mushroom body beta-lobe phenotype of DAAMEx1

Rac1J11/Rac1[+] is an enhancer of mushroom body phenotype of PsGEFΔ21

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of cone cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.UAS

Rac1J11 is an enhancer of neuropil phenotype of DAAMEx68

Rac1J11 is an enhancer of fascicle phenotype of DAAMEx68

Rac1J11 is an enhancer of connective phenotype of DAAMEx68

Rac1J11 is an enhancer of embryo phenotype of DAAMEx68

Rac1J11/Rac2Δ is an enhancer of neuropil phenotype of DAAMEx68

Rac1J11/Rac2Δ is an enhancer of fascicle phenotype of DAAMEx68

Rac1J11/Rac2Δ is an enhancer of connective phenotype of DAAMEx68

Rac1J11/Rac2Δ is an enhancer of embryo phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of neuropil phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of fascicle phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of connective phenotype of DAAMEx68

Rac1J11, Rac2Δ, MtlΔ is an enhancer of embryo phenotype of DAAMEx68

Rac1J11/Rac1[+] is an enhancer of ventral adult lateral neuron & commissure phenotype of Fmr1Δ113M

Rac1J11/Rac1[+] is an enhancer of LNv neuron phenotype of Fmr1Δ113M

NOT Enhancer of
Statement
Reference

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac1J11/Rac1[+] is a non-enhancer of leg phenotype of Sb70

Rac1J11/Rac1[+] is a non-enhancer of leg phenotype of br1

Rac1J11/Rac1[+] is a non-enhancer of leg phenotype of Sb63b

Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of photoreceptor cell & axon phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Rac1J11/Rac1[+] is a non-suppressor of wing phenotype of HIV-1\VpuUAS.cLa, Scer\GAL4dpp.blk1

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of wing phenotype of HIV-1\VpuUAS.cLa, Scer\GAL4dpp.blk1

Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

Rac1J11, Rac2Δ, MtlΔ is a non-suppressor of photoreceptor cell & axon phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549

Other
Statement
Reference

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+], sickΔ, tsr[+]/tsrN96A has mushroom body beta-lobe phenotype

Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+], shi2 has presumptive embryonic salivary gland | heat sensitive phenotype

MtlΔ, Rac1J11, Rac2Δ has embryonic leading edge cell & actin filament phenotype

Rac1J11, cdiR47/cdi[+] has testis phenotype

MtlΔ, Rac1J11, Rac2Δ has photoreceptor cell & axon phenotype

Rac1J11, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+] has adult mushroom body phenotype

Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ has adult mushroom body phenotype

Mtl[+]/MtlΔ, Rac1J11, Rac2Δ/Rac2[+] has adult mushroom body phenotype

Additional Comments
Genetic Interactions
Statement
Reference

The dot-like small eye phenotype characteristic for flies expressing egrScer\UAS.cMa under the control of Scer\GAL4GMR.PFa is partially suppressed by combination with Rac1J11 in heterozygous state.

One copy of Rac1J11 enhances the axonal growth defects seen in the α and β lobes of DAAMEx1 mutant mushroom bodies.

Hemizygous dsh1 mutant males with one copy of Rac1J11 exhibit an early growth termination phenotype in the mushroom body axons that is not observed in either dsh1/Y or Rac1J11/+ males alone.

Hemizygous Rac1J11 partially suppresses the medial lobe fusion phenotype seen when VangScer\UAS.T:Avic\GFP-m6 is expressed in male flies under the control of Scer\GAL4ey-OK107.

Hemizygous Rac1J11 partially suppresses the medial lobe fusion phenotype seen when Wnt5Scer\UAS.cFa is expressed in male flies under the control of Scer\GAL4ey-OK107.

Pupal retina constituting almost entirely of somatic clones (induced specifically in the eye) triple homozygous for Rac2Δ,Rac1J11,MtlΔ do not show any extra cone cells or primary pigment cells, only extra inter-ommatidial cells are observed.

Rac1J11/Rac1J10, Rac2Δ, MtlΔ triple mutant larvae exhibit strong ECM detachment and epithelial enclosure of dendrites in class IV dendritic arborizing neurons.

RetC168 Rac1J11 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite-ECM interaction. The phenotype is not observed in either heterozygote alone.

mew1 Rac1J11 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite-ECM interaction. The phenotype is not observed in either heterozygote alone.

mys1 Rac1J11 transheterozygous third instar larvae exhibit defects in class IV dendritic arborizing neuron dendrite-ECM interaction. The phenotype is not observed in either heterozygote alone.

The mushroom bodies of Rac1J11 Rac2Δ MtlΔ triple heterozygotes display short α/β axonal lobes compared with those of controls. The peduncle and ellipsoid body form normally.

The mushroom body axons of flies that are heterozygous for Rac1J11, Rac2Δ tsrN96A sickΔ and MtlΔ fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype).

The presence of Rac2Δ/+, Rac1J11/+ and MtlΔ/+ mutations 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.

Only small amounts of muscle fibers form in Rac1J11, Rac2Δ mutant embryos - these myofibers round up upon muscle contraction, indicating detachment.

Co-expression of Ced-12Scer\UAS.cGa and mbcScer\UAS.cBa via Scer\GAL4Mef2.PR results in prevalent myoblast fusion, muscle attachment, and tendon cell identity phenotypes in embryos. The muscle attachment and tendon cell phenotypes are largely rescued in a Rac1J11/+, Rac2Δ/+ background.

Myoblast fusion is defective in Rac1J11 Rac2Δ double mutant embryos, although some fusion does occur. Binucleate muscle precursors that have undergone a single fusion event between a founder cell and a fusion competent myoblast are seen in the mutant embryos as follows: DA1 (64.2% of segments), DO1 (68.3% of segments), LO1 (26.3% of segments), VT1 (66.7%) of segments.

A mild, though not significant enhancement of the ommatidium-phenotype resulting from the co-expression of Arf51FGD13822 with Dcr-2Scer\UAS.cDa under the control of Scer\GAL4GMR.PF is observed in a Rac1J11, Rac2Δ, MtlΔ heterozygous background.

Expression of psidinScer\UAS.cKa under the control of Scer\GAL4slbo.2.6 in a Rac1J11 Rac2Δ double heterozygous background has little or no effect on border cell migration.

No rhabdomeric defect is seen at the base of the rhabdomere at eclosion in flies in which the eyes are triply mutant for Rac1J11 Rac2Δ MtlΔ, although there is an axon guidance defect in the optic lobe.

The Rac1J11/+ heterozygous mutation causes a mild suppression of the GluRIIASP16 NMJ synaptic homeostatic response.

The ExnEY01953/+ heterozygous mutation does not enhance the Rac1J11/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype.

Larval hemocytes prepared from flies simultaneously heterozygous for drprΔ5, Rac1J11 and Rac2Δ show a significant reduction in the level of phagocytosis of S. aureus.

Heterozygosity for Rac1J11 enhances the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEFΔ21 animals; a pair of alpha/beta lobes is missing in 90% of the double mutants.

prtpΔ1/+ ; Rac1J11 Rac2Δ/+ triple heterozygotes show a reduced level of phagocytosis in embryonic hemocytes (neither prtpΔ1/+ single heterozygotes nor Rac1J11 Rac2Δ/+ double heterozygotes show a reduction in phagocytosis compared to wild type).

The rough eye phenotype resulting from Scer\GAL4GMR.PU-mediated expression of Ced-12Scer\UAS.cGa and mbcScer\UAS.cBa is suppressed by heterozygosity for Rac1J11, Rac2Δ.

A Rac1J11 Rac2Δ MtlΔ heterozygous background enhances the patterning defects found in Scer\GAL4GMR.PF>cindrdsRNA.PC.PD.Scer\UAS mutants. The mean interommatidial precursor cell number and the number of cone and/or 1[o] cell errors is increased in these double mutants.

The Scer\GAL4elav-C155/DAAMC.Scer\UAS.P\T gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is not affected by Rac1 gene dose (i.e. a Rac1J11/+ or Rac1J11/Rac1J10 background), a Rac1J11, Rac2Δ background or a Rac1J10, Rac2Δ, MtlΔ background.

A Rac1J11 background enhances the zygotic DAAMEx68 CNS phenotype, with the severity of the phenotype correlating with the number of Rac1 copies removed. A DAAMEx68 heterozygous background strongly enhances the axonal growth defects exhibited by Rac1J11 mutants.

A Rac1J11/+; Rac2Δ/+ background enhances both the zygotic DAAMEx68 and DAAMEx68; Rac1J11/+ CNS phenotypes.

A Rac1J11; Rac2Δ, Mtl[Δ] heterozygous background enhances the zygotic DAAMEx68, DAAMEx68; Rac1J11/+ and DAAMEx68; Rac1J11/+; Rac2Δ/+CNS phenotypes.

The increased bouton number at the neuromuscular junction that is seen in Vps35EY14200/Df(2R)ED3952 larvae is suppressed by Rac1J11/+.

Rac1J11, Rac2Δ, MtlΔ triple mutant clones in the eye result in a low frequency (approximately 5%) of planar polarity defects (such as achiral or misrotated ommatidia). Cdc425, Rac1J11, Rac2Δ, MtlΔ quadruple mutant clones in the eye result in a higher frequency of (14.2%) of planar polarity defects.

Rac1J11 Rac2Δ MtlΔ triple mutant myoblasts show enlarged foci, as well as increased numbers of actin foci. Enlarged foci are seen in these mutants from the earliest stages of fusion and foci persist after fusion would be complete in wild-type.

The salivary gland defects seen in Rac1J11 embryos are enhanced in Rac1J11 Rac2Δ mutants; more cells remain at the ventral surface of the embryo and the gland fails to migrate posteriorly. In addition, the lumen of the salivary gland is disrupted, with breaks in the lumen being seen during posterior migration of the gland, and cyst-like lumena being seen in the mature gland.

shi2 Rac1J11 Rac2Δ MtlΔ heterozygous embryos form normal salivary glands at the permissive temperature of 25[o]C. However, at the restrictive temperature of 30[o]C, posterior migration of the salivary gland is disrupted.

The Rac1J11 mutation fails to modify the cv-cM62 phenotype in the Malpighian tubules. Dorsal closure defects occur in 82% of Rac1J11, Rac2Δ double mutant embryos. If these mutants also carry the cv-cM62 mutation , 37 % of these embryos are rescued. In cv-cM62, Rac1J11, Rac2Δ triple mutants, the posterior spiracle phenotype is enhanced compared to cv-cM62 mutants. Posterior spiracle phenotypes are seen in Rac1J11, Rac2Δ embryos, but with low penetrance.

A Rac1J11/+ background enhances the splitting wing hair phenotype of flies that express trcT453A.Scer\UAS under the control of Scer\GAL4ap-md544.

In Rac1J11; Rac2Δ double homozygous embryos, rearrangement of tubule cells to produce elongated, 2 cell wide tubules is partially disrupted and tubule migration is defective. The anterior tubules follow an erratic path, doubling back on themselves to form loops and knots.

The penetrance of the LNv ectopic branch phenotype is increased to 100% and the posterior tract defasciculation phenotype is increased to 93% when Fmr1Δ113M/+ flies are also heterozygous for Rac1J11. Likewise, the LNv ectopic branch phenotype is increased to 100% and the posterior tract defasciculation phenotype is increased to 93% when Rac1J11/+ flies are also heterozygous for Fmr1Δ113M.

Both Rac1J11, Rac2Δ/Rac2Δ mutants and Rac2Δ, Rac1J11/Rac1J11 mutants show a reduction of 5-HT arborization in the larval brain.

Developmental dispersal of hemocytes is abnormal in embryos triply mutant for Rac1J11, Rac2Δ and MtlΔ.

One hour after laser-induced wounding, approximately half the number of hemocytes are recruited to the wound in embryos triply mutant for Rac1J11, Rac2Δ and MtlΔ compared to wild type embryos. Hemocytes that are recruited in the triple mutant embryos have significantly reduced lamellar protrusions.

Germ line clones of the Rac1J11 Rac2Δ MtlΔ triple mutant fail to produce embryos. Zygotic Rac1J11 Rac2Δ MtlΔ triple mutants, that have wild-type maternal contribution of Rac1, survive beyond early dorsal closure, but still show 100% embryonic lethality. These embryos achieve dorsal closure, but show puckering along the dorsal side. The dorsal hole becomes a long slit-like shape as it closes in the triple mutants, while the hole has an oval shape in wild-type embryos. Although amnioserosa cells are significantly larger in the mutants than in wild type, these cells are able to contract at a similar rate to wild type. The leading edge of zygotic Rac1J11 Rac2Δ MtlΔ triple mutants is disorganized and, unlike in wild-type embryos, is not taut. Many of the triple mutant leading edge cells are polygonal in shape, instead of being dorsally-ventrally elongated, like in wild type. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Leaky expression of hepCA.Scer\UAS, with no GAL4 driver, partially rescues the lethality and dorsal puckering phenotype of Rac1J11 Rac2Δ MtlΔ triple mutants.

Rac1J11/+ has very little effect on the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is 23% compared to 9% for control flies expressing LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E in an otherwise wild-type background). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is not increased if the flies are also heterozygous for Rac1J11/+ (3%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is not increased if the flies are also heterozygous for Rac1J11/+ (2%). The frequency of the malformed leg phenotype seen in br1/Y males (1%) is not increased if the flies are also heterozygous for Rac1J11/+ (0%).

Rac1J11, Rac2Δ mutant embryos exhibit arrested ganglionic branches (GBs), and GBs turning prematurely away from the midline. robo4 partially suppresses the ganglionic branch phenotype seen in Rac1J11, Rac2Δ embryos.

74% of Rac1J11 cdiR47/Rac1J11 males are sterile in individual crosses with females. The males have an abnormal accumulation of dense material in the distal part of the testis.

Double mutant clones of Rac1J11 and Rac2Δ do not affect F-actin enrichment in rhabdomeres.

In a subset of the epidermal cells of stage 15 Rac1J11, Rac2Δ double homozygous embryos, the distinction between apical and basolateral domains is compromised. At stage 16 the columnar epithelial cells are shorter than wild-type and parts of the epidermis become multilayered. Reducing the maternal and zygotic gene dosage of Rac1J11 and Rac2Δ together produces embryos exhibiting tracheal defects of increasing severity: the mildest phenotype is a mis-routing of the dorsal branches toward the anteroposterior direction, whereas more severely affected embryos also exhibit truncations of the dorsal trunk. Order of severity: maternal(M) +/+ zygotic(Z) +/- =WT. M -/+ Z +/+ < M -/+, Z -/+ < M +/-, Z -/-. The proportion of M -/+, Z -/+ embryos with severely affected tracheal systems is enhanceable by heterozygosity for bnl00857, btlΔOh10, or stumps09904b.

In a subset of the epidermis of stage 15 Rac1J11, Rac2Δ double homozygous embryos the distinction between apical and basolateral domains is compromised. At stage 16 the columnar epithelial cells are shorter than wild-type and parts of the epidermis become multilayered. Reducing the maternal and zygotic gene dosage of Rac1J11 and Rac2Δ together produces embryos exhibiting tracheal defects of increasing severity: The mildest phenotype is a misrouting of the dorsal branches toward the anteroposterior direction, whereas more severely effected embryos also exhibit truncations of the dorsal trunk. Order of severity: maternal(M) +/+ zygotic(Z) +/- =WT. M -/+ Z +/+ < M -/+, Z -/+ < M +/-, Z -/-. The proportion of M -/+, Z -/+ embryos with severely effected tracheal systems is enhanceable by heterozygosity for bnl00857, btlΔOh10, or stumps09904b.

The combination of heterozygous sli2 and Rac1J11 leads to an enhancement of the longitudinal axon ectopic midline crossing defects. An average of 4.8 defects are seen per animal, and an average of 44% of segments have defects.

Rac1J11 Rac2Δ MtlΔ triple mutant clones in the wing and eye do not show planar cell polarity defects. Mosaic flies in which the eye is doubly mutant for Rac1J11 and Rac2Δ show mild defects in the projection pattern of photoreceptor cell axons. Mosaic flies in which the eye is triply mutant for MtlΔ, Rac1J11 and Rac2Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. Specification of photoreceptor cell fate appears to be normal.

55% of Rac1J11 Rac2Δ double mutant neuroblast clones show defective guidance. 55% of Rac1J11 Rac2Δ MtlΔ single-cell γ neuron clones in the mushroom body show axon-stalling defects, mostly at the peduncle. There is a significant reduction in total dendritic length and number of dendritic segments per neuron compared to wild type. Mushroom body axon growth defects in single-cell Rac1J11 Rac2Δ MtlΔ γ neuron clones are largely rescued by expression of Rac1Scer\UAS.T:Hsap\MYC or Rac1Y40C.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107. Mushroom body axon growth defects in single-cell Rac1J11 Rac2Δ MtlΔ γ neuron clones are not rescued by expression of Rac1F37A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107. 81% of axons in Rac1J11 Rac2Δ mushroom body clones show mutant phenotypes, predominantly guidance (55%) and branching (24%) defects. Expression of Rac1Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107 markedly rescues these defects. Expression of Rac1Y40C.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4OK107 does not reduce the total percentage of axonal defects in Rac1J11 Rac2Δ mushroom body clones, but results in a marked shift in the distribution of defects, with most showing branching (45%) rather than guidance (31%) defects. Analysis of Rac1J11 Rac2Δ mushroom body clones indicates cell non-autonomous effects in axon guidance and branching caused by defective "Rac" activity.

The phenotype caused by expression of msnEP549 under the control of Scer\GAL4GMR.PF is not modified by the addition of the triple mutant combination Rac1J11 Rac2Δ MtlΔ.

Xenogenetic Interactions
Statement
Reference

Rac1J11/+ does not suppress the wing defects caused by expression of HIV-1\VpuScer\UAS.cLa under the control of Scer\GAL4dpp.blk1.

The presence of Rac1J11/+ and Rac2Δ/+ in double heterozygous combination does not suppress the wing defects caused by expression of HIV-1\VpuScer\UAS.cLa under the control of Scer\GAL4dpp.blk1.

Complementation and Rescue Data
Rescued by
Comments

Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4sns.PK strongly rescues the myoblast fusion defects of Rac1J11 Rac2Δ double mutant embryos, resulting in a near normal somatic muscle pattern. In contrast, expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4kirre-rP298 rescues the myoblast fusion defects of Rac1J11 Rac2Δ double mutant embryos much less efficiently.

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Stocks (3)
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References (60)