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General Information
Symbol
Dmel\Rac1J10
Species
D. melanogaster
Name
FlyBase ID
FBal0135836
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C1302246T

Amino acid change:

P34L | Rac1-PA; P34L | Rac1-PB

Reported amino acid change:

P?L

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: P?L.

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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

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

Embryos lacking both maternal and zygotic Rac1 function complete dorsal closure. Myoblast fusion appears complete in these embryos. Less than 2% of Rac1J10 mutant embryos show midline guidance defects (Fas2-positive longitudinal axons crossing the midline).

Homozygous adults show defects in branching of the mushroom body axons.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is an enhancer of partially lethal - majority die phenotype of slprBS06

NOT Enhancer of
Statement
Reference

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

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 abnormal neuroanatomy | 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

Rac1J10/Rac1[+] is a suppressor of abnormal neuroanatomy phenotype of hep1

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

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

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

NOT Suppressor of
Statement
Reference

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

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

Other
Phenotype Manifest In
Enhancer of
NOT Enhancer of
Suppressor of
Statement
Reference

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

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

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

Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1J10, Rac1[+] is a suppressor of larval 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

Rac1J10/Rac1[+] is a suppressor of axon & dorsal cluster neuron phenotype of hep1

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

Rac1J10/Rac1[+], Rac2Δ, Rac2Δ, Rac2[+], Rac2[+] is a suppressor of eye 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

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

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

Rac1J10/Rac1J10 is a suppressor of photoreceptor cell & axon phenotype of trioGEF1.GMR.Tag:MYC

NOT Suppressor of
Statement
Reference

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

Other
Statement
Reference

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, Rac1J10, Rac2Δ has photoreceptor cell & axon phenotype

MtlΔ, Rac1J10 has photoreceptor cell & axon phenotype

Rac1J10, Rac2Δ has photoreceptor cell & axon 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 Rac1J10, together with Rac2Δ and MtlΔ, all in heterozygous state.

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

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.

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.

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 suppresses 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 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/Rac1J10 background).

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

Rac1J10/+ suppresses the decrease in dorsal cluster neuron axon extension of hep1 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.

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.

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 MtlΔ double mutant embryos (lacking both maternal and zygotic function of the Rac1 and Mtl genes) show dorsal closure defects. Myoblast fusion appears complete in these embryos. 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. Rac1J10 enhances the frequency of midline guidance defects in MtlΔ mutant embryos to 75%. Axon stalling is occasionally seen in the double mutant embryos. 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 MtlΔ and Rac1J10 show defects in the projection pattern of photoreceptor cell axons, showing a medulla bypass phenotype. 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.

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

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (27)