Allele Dmel\Rac1J11
| General Information | |||
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| Symbol | Dmel\Rac1J11 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0135835 | |
| Feature type | allele | Associated gene | Dmel\Rac1 |
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| Allele class | loss of function allele | ||
| Mutagen | ethyl methanesulfonate | ||
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| FB2013_03 | |||
| FB2013_02 |
Controlled Vocabulary Terms
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| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References point mutation pr_change=G60E|Rac1-PA evidence=experimental comment=Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. reported_pr_change=G?E na_change=G1302168A | |||
| Associated Sequence Data | |||
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
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| Progenitor genotype | |||
| Nature of the lesion | Statement Reference Amino acid replacement: G60E. | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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axon & dorsal cluster neuron | somatic clone ventral adult lateral neuron & commissure | |||
Detailed Description
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Statement Reference 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. The salivary gland cells invaginate in Rac1[J11] 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
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Interactions
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Phenotypic Class
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Enhanced by | |||
Statement Reference | |||
NOT Enhanced by | |||
Statement Reference GluRIIASP16, Rac1J11/Rac1[+] has neurophysiology defective | recessive | third instar larval stage phenotype, non-enhanceable by ExnEY01953/Exn[+] | |||
Suppressed by | |||
Statement Reference MtlΔ, Rac1J11, Rac2Δ has lethal | embryonic stage phenotype, suppressible | partially by hepCA.Scer\UAS/Scer\GAL4[-] | |||
Enhancer of | |||
Statement Reference Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of planar polarity defective phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS Rac1J11/Rac1[+] is an enhancer of neuroanatomy defective phenotype of LIMK1Scer\UAS.T:Ivir\HA1, Scer\GAL4ey-OK107 Rac1J11/Rac1[+] is an enhancer of planar polarity defective phenotype of MtlScer\UAS.cMa, Scer\GAL4hs.2sev | |||
NOT Enhancer of | |||
Statement Reference Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of neuroanatomy defective phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of neuroanatomy defective phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549 Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11/Rac1J10 is a non-enhancer of neuroanatomy defective phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac2Δ is a non-enhancer of neuroanatomy defective phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11 is a non-enhancer of neuroanatomy defective phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 | |||
NOT Suppressor of | |||
Statement Reference Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11, Rac2Δ, MtlΔ is a non-suppressor of neuroanatomy defective phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549 Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of HIV-1\VpuScer\UAS.cLa, Scer\GAL4dpp.blk1 Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-suppressor of visible phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11/Rac1[+] is a non-suppressor of visible phenotype of HIV-1\VpuScer\UAS.cLa, Scer\GAL4dpp.blk1 | |||
Other | |||
Statement Reference GluRIIASP16, Rac1J11/Rac1[+], cacS/cac[+] has neurophysiology defective | recessive | third instar larval stage phenotype GluRIIASP16, Rac1J11/Rac1[+] has neurophysiology defective | recessive | third instar larval stage phenotype | |||
Phenotype Manifest In
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Enhanced by | |||
Statement Reference 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 has ventral adult lateral neuron & commissure phenotype, enhanceable by Dp(2;2)C619/+ | |||
NOT Enhanced by | |||
Statement Reference GluRIIASP16, Rac1J11/Rac1[+] has embryonic/larval neuromuscular junction phenotype, non-enhanceable by ExnEY01953/Exn[+] | |||
Suppressed by | |||
Statement Reference MtlΔ, Rac1J11, Rac2Δ has dorsal closure embryo phenotype, suppressible | partially by hepCA.Scer\UAS/Scer\GAL4[-] MtlΔ, Rac1J11, Rac2Δ has embryonic/first instar larval cuticle phenotype, suppressible | partially by hepCA.Scer\UAS/Scer\GAL4[-] | |||
Enhancer of | |||
Statement Reference Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of cone cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is an enhancer of pigment cell phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.PC.PD.Scer\UAS Rac1J11/Rac1[+] is an enhancer of adult mushroom body phenotype of LIMK1Scer\UAS.T:Ivir\HA1, Scer\GAL4ey-OK107 Rac1J11/Rac1[+] is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4ap-md544, trcT453A.Scer\UAS | |||
NOT Enhancer of | |||
Statement Reference Rac1J11, MtlΔ, Rac1J10 is a non-enhancer of fascicle | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11, Rac2Δ, Mtl[+], MtlΔ, Rac2[+], Rac1[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of commissure | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of fascicle | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of neuropil | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11, Rac2Δ, MtlΔ is a non-enhancer of photoreceptor cell & axon phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, msnEP549 Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053 Rac1J11/MtlΔ is a non-enhancer of fascicle | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac1J10, Scer\GAL4elav-C155 is a non-enhancer of neuropil | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac1J10 is a non-enhancer of commissure | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac2Δ is a non-enhancer of commissure | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac2Δ is a non-enhancer of fascicle | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11/Rac2Δ is a non-enhancer of neuropil | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11 is a non-enhancer of commissure | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 Rac1J11 is a non-enhancer of neuropil | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155 | |||
Suppressor of | |||
Statement Reference Rac1J11, Rac2Δ, Rac2[+], Rac1[+] is a suppressor of eye phenotype of Ced-12Scer\UAS.cGa, Scer\GAL4Mef2.PR, mbcScer\UAS.cBa | |||
NOT Suppressor of | |||
Statement Reference Rac1J11, Rac2Δ, Mtl[+], MtlΔ, 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 Rac1J11, Rac2Δ, 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 phenotype of HIV-1\VpuScer\UAS.cLa, Scer\GAL4dpp.blk1 | |||
Other | |||
Statement Reference Mtl[+]/MtlΔ, Rac1J11/Rac1[+], Rac2Δ/Rac2[+], shi2 has presumptive embryonic salivary gland | heat sensitive phenotype | |||
Additional Comments
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Genetic Interactions
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Statement Reference Myoblast fusion is defective in Rac1[J11] Rac2[Δ] 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 Arf51F[GD13822] with Dcr-2[Scer\UAS.cDa] under the control of Scer\GAL4[GMR.PF] is observed in a Rac1[J11], Rac2[Δ], Mtl[Δ] heterozygous background. Expression of psidin[Scer\UAS.cKa] under the control of Scer\GAL4[slbo.2.6] in a Rac1[J11] Rac2[Δ] double heterozygous background has little or no effect on border cell migration. The Rac1[J11]/+ heterozygous mutation causes a mild suppression of the GluRIIA[SP16] NMJ synaptic homeostatic response.
The Exn[EY01953]/+ heterozygous mutation does not enhance the Rac1[J11]/+, GluRIIA[SP16] double mutant NMJ synaptic homeostasis phenotype. Heterozygosity for Rac1[J11] enhances the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEF[Δ21] animals; a pair of alpha/beta lobes is missing in 90% of the double mutants. The rough eye phenotype resulting from Scer\GAL4[GMR.PU]-mediated expression of Ced-12[Scer\UAS.cGa] and mbc[Scer\UAS.cBa] is suppressed by heterozygosity for Rac1[J11], Rac2[Δ]. A Rac1[J11] Rac2[Δ] Mtl[Δ] heterozygous background enhances the patterning defects found in Scer\GAL4[GMR.PF]>cindr[dsRNA.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\GAL4[elav-C155]/DAAM[C.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 Rac1[J11]/+ or Rac1[J11]/Rac1[J10] background), a Rac1[J11], Rac2[Δ] background or a Rac1[J10], Rac2[Δ], Mtl[Δ] background.
A Rac1[J11] background enhances the zygotic DAAM[Ex68] CNS phenotype, with the severity of the phenotype correlating with the number of Rac1 copies removed. A DAAM[Ex68] heterozygous background strongly enhances the axonal growth defects exhibited by Rac1[J11] mutants.
A Rac1[J11]/+; Rac2[Δ]/+ background enhances both the zygotic DAAM[Ex68] and DAAM[Ex68]; Rac1[J11]/+ CNS phenotypes.
A Rac1[J11]; Rac2[Δ], Mtl[Δ] heterozygous background enhances the zygotic DAAM[Ex68], DAAM[Ex68]; Rac1[J11]/+ and DAAM[Ex68]; Rac1[J11]/+; Rac2[Δ]/+CNS phenotypes. The increased bouton number at the neuromuscular junction that is seen in Vps35[EY14200]/Df(2R)ED3952 larvae is suppressed by Rac1[J11]/+. Rac1[J11], Rac2[Δ], Mtl[Δ] triple mutant clones in the eye result in a low frequency (approximately 5%) of planar polarity defects (such as achiral or misrotated ommatidia). Cdc42[5], Rac1[J11], Rac2[Δ], Mtl[Δ] quadruple mutant clones in the eye result in a higher frequency of (14.2%) of planar polarity defects. The salivary gland defects seen in Rac1[J11] embryos are enhanced in Rac1[J11] Rac2[Δ] 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.
shi[2] Rac1[J11] Rac2[Δ] Mtl[Δ] 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. 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. 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%). 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. 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. 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
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Statement Reference Rac1[J11]/+ does not suppress the wing defects caused by expression of HIV-1\Vpu[Scer\UAS.cLa] under the control of Scer\GAL4[dpp.blk1].
The presence of Rac1[J11]/+ and Rac2[Δ]/+ in double heterozygous combination does not suppress the wing defects caused by expression of HIV-1\Vpu[Scer\UAS.cLa] under the control of Scer\GAL4[dpp.blk1]. | |||
Complementation & Rescue Data
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| Rescued by | |||
| Comments | Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[sns.PK] strongly rescues the myoblast fusion defects of Rac1[J11] Rac2[Δ] double mutant embryos, resulting in a near normal somatic muscle pattern. In contrast, expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[kirre-rP298] rescues the myoblast fusion defects of Rac1[J11] Rac2[Δ] double mutant embryos much less efficiently. | ||
Stocks
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| Bloomington | |||
Notes on Origin
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External Crossreferences & Linkouts
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Synonyms & Secondary IDs
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| Reported As | |||
| Symbol Synonym | Drac1J11 rac1J11 Rac1J11 (Stramer et al., 2005, Puetz et al., 2005, Johnson et al., 2011, Pirraglia et al., 2006, Avet-Rochex et al., 2007, Korolchuk et al., 2007, Sampson et al., 2012, Rothenfluh et al., 2006, Frank et al., 2009, Geisbrecht et al., 2008, Kuraishi et al., 2009, Paladi and Tepass, 2004, Djiane and Mlodzik, 2010, Matusek et al., 2008, Richardson et al., 2007, Muñoz-Descalzo et al., 2007, Hashimoto et al., 2009) | ||
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References
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Recent research papers ( 6 ) | |||
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