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General Information
Symbol
Dmel\Rac2Δ
Species
D. melanogaster
Name
FlyBase ID
FBal0135831
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
rac2
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the P{PZ} element resulting in a deletion that disrupts the Rac2 open reading frame.

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

Rac2Δ mutant males appear thinner than equally-aged controls. Their abdomens, in particular, appear thinner than in controls.

Rac2Δ homozygous males perform significantly more wing flicks over a 20 minute fighting bout than controls or heterozygous males. On the other hand, Rac2Δ homozygous males perform significantly fewer leg shoves than controls.

Rac2Δ homozygous and heterozygous males perform significantly more singing behaviours and circling manoeuvres than controls, and unlike controls they perform abdomen bends towards other males. In terms of individual courtship behaviour, Rac2Δ mutants display all the behaviours males would normally present towards virgin females, including, singing, circling, tapping of the abdomen, licking the genitalia and bending their abdomen.

While Rac2Δ mutant males perform significantly more courtship behaviours than controls, they are not any less aggressive. However, the courting, or following, male never initiates aggressive interactions.

Homozygous larvae fail to encapsulate eggs of the avirulent wasp strain L. boulardi G486.

Isolated plasmatocytes from homozygous larvae show a reduced ability to phagocytose E. coli and S. aureus in a phagocytosis assay.

The ultrastructure of Rac2Δ mutant photoreceptor cells closely resemble wild-type.

Elctroretinograms (ERGs) of Rac2Δ/Df(3L)pbl-X1 and homozygous Rac2Δ mutant flies show abnormal termination rates of the photoresponse. The mutant retinae show impaired ability to undergo rapid response termination after pre-exposure to light.

Homozygous Rac2Δ adults do not display any obvious eye phenotypes.

Homozygous and Rac2Δ/Df(3L)pbl-X1 flies show strong sensitivity to infection with P.aeruginosa by septic injury. Homozygous flies also show reduced survival to oral infection with P.aeruginosa compared to control flies.

Homozygous flies show sensitivity to infection with E.cloacae, A.tumefaciens, S.aureus or E.faecalis by septic injury.

Homozygous flies are not sensitive to infection with E.coli by septic injury.

Circulating plasmatocytes from third instar Rac2Δ larvae show a reduction in phagocytic index (for dead E.coli and dead S.aureus) compared to control plasmatocytes.

Rac1J11 Rac2Δ MtlΔ triple mutants 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.

Disruption of the 5-HT arborization is observed in 37% of Rac2Δ larval brains.

0% of homozygous and Rac2Δ/Rac2KG05681b larvae show proper encapsulation (seen as a dark capsule around the egg) of wasp eggs (avirulent L.boulardi wasp strain G486) 40-42 hours after parasitisation, in contrast to heterozygous control larvae where 71.2% (Rac2Δ/+) and 89.4% (Rac2KG05681b/+) of the wasps eggs are properly encapsulated at this time. Improperly encapsulated wasp eggs can be recovered from Rac2Δ homozygous larvae, but there is no darkening of the capsule surrounding the wasp egg and there is no separation between the wasp embryo and the chorion/hemocyte capsule in contrast to that seen in encapsulated wasp eggs in wild-type larvae.

The number of crystal cells in homozygous larvae is comparable to that of controls.

Hemocytes recovered from Rac2Δ homozygous larvae that have been parasitised by L.boulardi are smaller and rounder in appearance than equally aged parasitised control hemocytes.

Plasmatocytes that have attached to wasp eggs in Rac2Δ homozygous larvae that have been parasitised by L.boulardi look completely different from those in their heterozygous parasitised controls; in the homozygous larvae, the plasmatocytes adhere to the wasp egg, but fail to spread around it. Similarly, lamellocytes are found adhered to the wasp egg in homozygous larvae, but they have a rounded form, instead of the spread appearance seen in control parasitised larvae. Circulating lamellocytes from homozygous larvae are capable of spreading on a glass surface as are control circulating lamellocytes.

The mesoderm flattens down onto the ectoderm in embryos lacking Rac2 function, but does not adhere to the ectoderm properly.

Mutant embryos have an increased number of muscle founder cells, leading to the formation of supernumerary muscle precursors and in consequence, increased numbers of small muscles. The muscle pattern is severely disorganised in late stage embryos. The population of eve-expressing pericardial cells and DA1 muscle founders is enlarged.

Homozygous mutant embryos show a lack of glial sheaths in the lateral region of PNS axonal tracts.

Embryos lacking both maternal and zygotic Rac2 function complete dorsal closure. A few isolated myoblasts fail to fuse in these embryos. Less than 2% of Rac2Δ mutant embryos show midline guidance defects (Fas2-positive longitudinal axons crossing the midline).

Homozygous adults show normal mushroom body axon patterning.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
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

Rac2Δ/Rac2[+] is a non-enhancer of visible | adult stage phenotype of Rac1J11/Rac1[+], Scer\GAL4GMR.PFa, egrUAS.cMa

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

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

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-enhancer of lethal | recessive | embryonic stage phenotype of arm8

Rac2Δ/Rac2[+] is a non-enhancer of neuroanatomy defective phenotype of PsGEFΔ21

Suppressor of
Statement
Reference

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor | partially of visible | adult stage phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor of visible | adult stage phenotype of Scer\GAL4GMR.PU, pblDH-PH.UAS.Tag:HA

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of chemical resistant phenotype of RhoGAP18B1

Rac2Δ, Rac2[+], Rac1J10, Rac1[+] is a suppressor | partially of neuroanatomy defective | somatic clone phenotype of ssh1-11

Rac2Δ, Rac2[+], Rac1J10, Rac1[+] is a suppressor | partially of neuroanatomy defective phenotype of PakUAS.Tag:MYC, Scer\GAL4ey-OK107

NOT Suppressor of
Statement
Reference

Rac2Δ/Rac2[+] is a non-suppressor of visible | adult stage phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

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

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-suppressor of lethal | recessive | embryonic stage phenotype of arm8

Rac2Δ/Rac2[+] is a non-suppressor of visible phenotype of Scer\GAL4GMR.PU, VavΔ1-207.UAS.Tag:HA

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of lethal | pharate adult stage | temperature conditional phenotype of Scer\GAL4GMR.PU, pblΔN-term.UAS.Tag:HA

Rac2Δ, Mtl[+], MtlΔ, Rac2[+] is a non-suppressor of neuroanatomy defective phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

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, 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, 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[+]

Suppressed by
Enhancer of
Statement
Reference

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/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

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

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

Rac2Δ, Rac1J6, Rac2[+], Rac1[+] is an enhancer of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

NOT Enhancer of
Statement
Reference

Rac2Δ/Rac2[+] is a non-enhancer of eye phenotype of Rac1J11/Rac1[+], Scer\GAL4GMR.PFa, egrUAS.cMa

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

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-enhancer of abdominal ventral denticle belt | embryonic stage phenotype of arm8

Rac2Δ/Rac2[+] is a non-enhancer of mushroom body alpha-lobe phenotype of PsGEFΔ21

Rac2Δ/Rac2[+] is a non-enhancer of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

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

Suppressor of
Statement
Reference

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor | partially of eye phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a suppressor of tendon cell | embryonic stage phenotype of Ced-12UAS.cGa, Scer\GAL4Mef2.PR, mbcUAS.cBa

Rac2Δ, MtlΔ, Rac1J10, Rac1[+] is a suppressor of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of segmental nerve branch SNa of A1-7 | heat sensitive phenotype of Nl1N-ts1

Rac2Δ, Mtl[+], Rac1J10, MtlΔ, Rac2[+], Rac1[+] is a suppressor of eye | adult stage phenotype of Scer\GAL4GMR.PU, pblDH-PH.UAS.Tag:HA

Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a suppressor of eye phenotype of Ced-12UAS.cGa, Scer\GAL4Mef2.PR, mbcUAS.cBa

Rac1J10/Rac1[+], Rac2Δ, Rac2Δ, Rac2[+], Rac2[+] is a suppressor of ommatidium phenotype of FBal0135831:/Rac2+ :, Scer\GAL4ey.PB, stidsRNA.Sym.UAS

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of eye & ommatidium phenotype of tumdsRNA.UAS.cBa, Scer\GAL4ey.PB

Rac1J10/Rac1[+], Rac2Δ, Rac2Δ, Rac2[+], Rac2[+] is a suppressor of eye phenotype of FBal0135831:/Rac2+ :, Scer\GAL4ey.PB, stidsRNA.Sym.UAS

Rac2Δ, Rac2[+], Rac1J10, Rac1[+] is a suppressor | partially of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

Rac2Δ, Rac2[+], Rac1J10, Rac1[+] is a suppressor | partially of adult mushroom body | somatic clone phenotype of ssh1-11

Rac2Δ, Rac2[+], Rac1J10, Rac1[+] is a suppressor | partially of adult mushroom body phenotype of PakUAS.Tag:MYC, Scer\GAL4ey-OK107

Rac2Δ/Rac2Δ is a suppressor of photoreceptor cell & axon phenotype of trioGEF1.GMR.Tag:MYC

NOT Suppressor of
Statement
Reference

Rac2Δ/Rac2[+] is a non-suppressor of eye phenotype of Scer\GAL4GMR.PFa, egrUAS.cMa

Rac1J11, Rac2Δ, Rac2[+], 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 hair phenotype of Scer\GAL4en-e16E, kermitGS2053

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

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a non-suppressor of abdominal ventral denticle belt | embryonic stage phenotype of arm8

Rac2Δ/Rac2[+] is a non-suppressor of eye phenotype of Scer\GAL4GMR.PU, VavΔ1-207.UAS.Tag:HA

Rac2Δ/Rac2[+] is a non-suppressor of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev

Rac2Δ, Mtl[+], MtlΔ, Rac2[+] is a non-suppressor of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107

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

MtlΔ, Rac1J10, Rac2Δ has embryonic leading edge cell & actin filament | germ-line clone phenotype

MtlΔ, Rac1J10, Rac2Δ has embryonic leading edge cell & actin filament phenotype

MtlΔ, Rac1J11, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac2Δ has photoreceptor cell & axon phenotype

Rac1J10, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J10, Rac2Δ has photoreceptor cell & axon phenotype

Rac1J11, Rac2Δ has photoreceptor cell & axon phenotype

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

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

Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ 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 cannot be suppressed by combination with Rac2Δ in heterozygous state.

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 Rac1J10, together with Rac2Δ and MtlΔ, all in heterozygous state.

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.

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).

After single cell wounding (by laser ablation), Rac triple mutant embryos (Rac1J10, Rac2Δ, MtlΔ) show severe disruption of actin cortical flow, affecting both actin ring and actin halo formation, resulting in wound overexpansion and an aberrant oval (rather than rounded) wound shape.

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.

ZirBG00267/+ ; Rac2Δ/+ double heterozygous larvae have a reduced rate of encapsulation (42%) of eggs of the avirulent wasp strain L. boulardi G486 compared to the rate seen in either single heterozygote.

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.

Heterozygosity for Rac1J10 Rac2Δ MtlΔ suppresses the axonal defects found in Nl1N-ts1 mutants.

Heterozygosity for a Rac1J10 Rac2Δ MtlΔ triple mutant chromosome does not alter arm8 mutant patterning nor its rate of hatching.

The eye phenotype seen when vavΔ1-207.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU is suppressed in a homozygous Rac2Δ background. The phenotype is not suppressed in a Rac2Δ/+ background.

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 Rac2Δ has no effect on the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEFΔ21 animals.

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).

One copy of each of Rac1J10, Rac2Δ and MtlΔ fails to suppress the lethality seen when pblΔN-term.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

One copy of each of Rac1J10, Rac2Δ and MtlΔ strongly supresses the rough eye phenotype seen when pblDH-PH.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

Stage 8 embryos lacking zygotic and maternal expression of Rac1J10, Rac2Δ and MtlΔ display mesoderm migration defects.

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 a Rac1J11, Rac2Δ background or a Rac1J10, Rac2Δ, MtlΔ background.

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.

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.

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.

Heterozygosity for Rac1J10 Rac2Δ MtlΔ suppresses the RhoGAP18B1 ethanol-resistance phenotype.

The Rac2Δ 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.

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.

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.

Contacts between the invaginated mesoderm and the ectoderm fail to be established properly in embryos derived from females with reduced Rac2 and Rac1 function. Contacts between the invaginated mesoderm and the ectoderm fail to be established properly in embryos derived from females with reduced Mtl, Rac2 and Rac1 function.

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 mutant 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. Rac1J10 Rac2Δ MtlΔ triple mutant germ line clone embryos exhibit failure in germband retraction, head involution and dorsal closure. Not all of these phenotypes are fully penetrant; embryos with the least severe phenotype show only failure in dorsal closure. The epithelial cells of these embryos lack both actin cables and actin protrusions at the leading edges. The leading edge of zygotic Rac1J10 Rac2Δ MtlΔ triple mutants is somewhat disordered. Some of the cells in the mutant edge assemble the actin cable and actin projections, while other cells fail to do so. Cells without protrusions halt the "zipper" that closes the dorsal hole. However, the mutant exhibits a compensatory mechanism in which new zippering fronts emerge after the actin deficient stretches to complete closure.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to almost completely dominantly suppress the stidsRNA.Sym.Scer\UAS (under the regulation of Scer\GAL4ey.PB) phenotype, reverting the eye to wild-type size and appearance. Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) are able to dominantly suppress the RacGAP50CdsRNA.Scer\UAS (under the regulation of Scer\GAL4ey.PB) eye phenotype.

Mosaic border follicle cell clusters, which contain some wild-type cells and some cells with the genotype Rac1J10 Rac2Δ MtlΔ/Rac1J10 Rac2Δ Mtl+ show impaired migration.

Rac1J11, Rac2Δ or 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.

Homozygous Rac1J10 Rac2Δ embryos derived from homozygous Rac1J10 Rac2Δ female germline clones show mild defects in macrophage migration as macrophages do not disperse into the ventral posterior trunk region by stage 14 or 15. By late embryogenesis, macrophages have dispersed throughout the entire ventral trunk in these embryos. Sibling embryos that are derived from homozygous Rac1J10 Rac2Δ female germline clones but are zygotically heterozygous for Rac1J10 Rac2Δ (having received a paternal wild-type copy of Rac1 and Rac2) show a normal distribution of macrophages.

Homozygous Rac1J10 Rac2Δ MtlΔ embryos derived from homozygous Rac1J10 Rac2Δ MtlΔ female germline clones show the same macrophage migration defects as homozygous Rac1J10 Rac2Δ embryos derived from homozygous Rac1J10 Rac2Δ female germline clones.

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

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. Rac1J11, Rac2Δ double homozygous embryos exhibit a variety of tracheal defects: 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.

The combination of heterozygous sli2 and Rac2Δ leads to longitudinal axon ectopic midline crossing defects. An average of 1.4 defects are seen per animal, and an average of 13% of segments have defects.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos (lacking both maternal and zygotic function of the Rac1, Rac2 and Mtl genes) fail to complete dorsal closure. There is little or no actin accumulation at the leading epidermal edge and both lamellipodia and filopodia are lacking. The underlying amnioserosa cells appear normal. Little or no myoblast fusion occurs in these embryos. Severe axon growth defects are seen; in the CNS, Fas2-positive axons rarely extend from one segment into the next and very few sensory axons from the PNS reach the CNS. Specification of neuronal and glial cell fate and dendritic growth and morphology appears relatively normal. Rac1J10 Rac2Δ double mutant embryos (lacking both maternal and zygotic function of the Rac1 and Rac2 genes) show dorsal closure defects. Little or no myoblast fusion occurs in these embryos. Rac2Δ MtlΔ double mutant embryos (lacking both maternal and zygotic function of the Rac2 and Mtl genes) successfully complete dorsal closure. A few isolated myoblasts fail to fuse in these embryos. Rac1J11 Rac2Δ MtlΔ triple mutant clones in the wing and eye do not show planar cell polarity defects. Rac2Δ enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 42%. Less than 2% of Rac1J10 Rac2Δ mutant embryos show midline guidance defects (Fas2-positive longitudinal axons crossing the midline). Mosaic flies in which the eye is doubly mutant for Rac1J10 and Rac2Δ show mild defects in the projection pattern of photoreceptor cell axons. 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 doubly mutant for MtlΔ and Rac2Δ show mild defects in the projection pattern of photoreceptor cell axons. Mosaic flies in which the eye is triply mutant for MtlΔ, Rac1J10 and Rac2Δ show severe defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. The projection defects in the triple mutant eyes can be rescued by Rac1GMR.PNe or MtlGMR.PN. 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.

Rac1J10 Rac2Δ MtlΔ triple mutant embryos exhibit no significant retardation of wound closure.

Xenogenetic Interactions
Statement
Reference

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.

Expression of Rac2Scer\UAS.cEa under the control of Scer\GAL4ninaE.PT rescues the defect in light adaptation as measured by electroretinograms (ERGs).

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