A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Rac1Scer\UAS.cLa

General Information
SymbolDmel\Rac1Scer\UAS.cLaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct of LuoFlyBase IDFBal0038995
Feature typealleleAssociated geneDmel\Rac1
Allele class
Mutagenin vitro construct - regulatory fusion
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Description
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FB2013_03
FB2013_02
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Construct: Rac1 is expressed under the influence of Scer\GAL4 via upstream UAS sequences.
Carried in construct
Cytology
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axon & dorsal cluster neuron, with Scer\GAL4ato.3.6
dendritic spine & lobular plate tangential neuron, with Scer\GAL4DB331
filopodium & dendrite, with Scer\GAL4109(2)80
multidendritic neuron & dendrite, with Scer\GAL4477
multidendritic neuron & dendrite | supernumerary, with Scer\GAL4477
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Class III ddaA neurons expressing Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[1003.3] show a dramatic increase in the number of dendritic sensory filopodia compared to wild type. These filopodia are dynamic and their stability is not altered compared to controls. The average length of the filopodia is significantly decreased compared to wild type, while the total length of primary dendritic branches is not altered. Larvae expressing Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[1003.3] are hypersensitive to gentle touch compared to controls.
Overexpression of Rac1[Scer\UAS.cLa] in many neuron types, including the da neurons, under the control of Scer\GAL4[477], leads to hyperbranching of dendrites.
Expression of Rac1[Scer\UAS.cLa] under the control of the neuronal drivers Scer\GAL4[BG380], Scer\GAL4[OK6] or Scer\GAL4[elav-C155] leads to neuromuscular junction overgrowth during larval development, resulting in an increase in the number of synaptic boutons, branches and the appearance of abnormal synaptic protrusions. No overgrowth is seen when Rac1[Scer\UAS.cLa] is expressed in muscle under the control of the Scer\GAL4[Mhc.PW] driver. Expression of Rac1[Scer\UAS.cLa] under the control of either Scer\GAL4[BG380] or Scer\GAL4[OK6] produces increased mean evoked excitatory junctional potentials (EJPs) and quantal content in third instar larvae compared to controls. The size of miniature excitatory junctional potentials (mEJPs) does not differ from controls.
Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[DB331] does not alter the overall dendritic architecture in the lobular plate tangential cells; neither the position not branching patterns of primary and secondary order dendrites are affected. However, there is an increase in spine density and a change in spine morphology (the spines appear shorter and less well defined) compared to controls.
Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[221] in class I neurons promotes de novo branch initiation reminiscent of, but not identical to, the filopodia of class III neurons.
Expression of Rac1Scer\UAS.cLa under the control of cer\GAL4ato.3.6 inhibits the extension of axons from dorsal cluster neurons (DCNs), with an average of only 7.8 axons crossing toward the medulla instead of the wild-type average of 11.7. Expression of this transgene also results in a decreased number of DCN axons crossing the optic chiasm at 20%-30% pupal development.
Expression of Rac1Scer\UAS.cLa, under the regulation of Scer\GAL4109(2)80, dramatic increases in larval neurons dendritic branching are observed. This is due to the formation of filopodia on normally non-filopodia bearing neurons (non-class III dendritic arborisation neurons), without altering the filopodia density. This branching phenotype becomes apparent in newly-hatched first instar larvae. Rac1Scer\UAS.cLa expression, under the regulation of Scer\GAL4109(2)80, like CaMKIIT287D.Scer\UAS expression, increases actin turnover, although the effects on morphological stability are significantly different.
Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[GMR.PF] results in about 90% pupal lethality. Escaper adults have strongly reduced eyes with no organised structure.
When Rac1Scer\UAS.cLa is driven by Scer\GAL4GMR.PF a rough eye phenotype is seen.
When Rac1Scer\UAS.cLa is driven by Scer\GAL4477, an overbranching phenotype is seen in class IV neurons.
Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4slbo.2.6 at 25oC does not alter the migration of border follicle cells that occurs during oogenesis.
When expression is driven by Scer\GAL4He.PZ, hemocyte proliferation and lamellocyte numbers are increased, and crystal cells are unaffected. Melanotic masses form. Similar, though milder, effects are seen when expression is driven by Scer\GAL4Hml.PG.
When driven by Scer\GAL4sca-109-68 bristle defects occur. When driven by Scer\GAL4109-69 eyes are roughened. Lethality, when driven by Scer\GAL4109-79 acts in the embryonic-larval stages.
Targeted expression of Rac1[Scer\UAS.cLa] to the GF under the control of Scer\GAL4[A307] results in over 95% of GF axons showing morphological aberrations whereas less than 15% of controls show defects. In the majority of specimens the axons grow out of the brain and into the second thoracic neuromere (T2) but fail to make the terminal bend that is characteristic of the gf presynatpic terminal. In addition the tips of the axons appear swollen and contain vesicle-like structures. Nine percent of axons fail to exit the brain and often cross the midline and project into the contralateral half of the brain. Over 90% of GFs in Scer\GAL4[A307]; Rac1[Scer\UAS.cLa] adult brains exhibit abnormalities. Although neurite outgrowth and branching appears normal, and the three major dendritic domains are always discernible, typically dendrite are thickened and display inappropriate minor branches. Swollen dendrites containing large vesicle-like structures are also observed. When Scer\GAL4[A307]; Rac1[Scer\UAS.cLa] flies are tested physiologically, they all exhibit a TTM response latency that is more than twice that of control flies. The fidelity of transmission for repetitive stimuli is also reduced and in most cases only a single response to the first stimulus occurs. Approximately 30% of Scer\GAL4[c17]; Rac1[Scer\UAS.cLa] GF axons exhibit a bendless phenotype with swollen terminals and no lateral bends while the remaining axons appear wild-type. Approximately 81% of Scer\GAL4[A307]; Rac1[Scer\UAS.cLa] flies exhibit a bendless GF phenotype, while 64% of Scer\GAL4[A307]; Rac1[Scer\UAS.cLa] GFs are bendless. The remainder exhibit wild-type bends or large abnormally shaped processes in the target region.
Expression is driven by Scer\GAL4en-e16E causes wing vein thickening, extra sensory organs and wing enlargement.
Scer\GAL4elav-C155-mediated expression does not affect the normal anatomy of the CNS pathways. Scer\GAL4elav-C155-mediated expression of Rac1L89.Scer\UAS slightly disrupts CNS axon pathway, gaps between segments suggest failure in axon extension. Coexpression of Rac1Scer\UAS.cLa under the same Scer\GAL4 driver causes a massive failure in axon extension, dramatically enhancing the effect of Rac1L89.Scer\UAS. Axons that do extend follow abnormal trajectories.
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Scer\GAL460/Rac1Scer\UAS.cLa is a non-enhancer of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1
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Rac1Scer\UAS.cLa, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-enhanceable by btlDN.Scer\UAS, Scer\GAL4ato.3.6
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Rac1Scer\UAS.cLa, Scer\GAL4477 has multidendritic neuron & dendrite | supernumerary phenotype, suppressible | partially by trcScer\UAS.T:Zzzz\FLAG, Scer\GAL4477
Rac1Scer\UAS.cLa, Scer\GAL4477 has multidendritic neuron & dendrite phenotype, suppressible | partially by trcScer\UAS.T:Zzzz\FLAG, Scer\GAL4477
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Rac1Scer\UAS.cLa, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-suppressible by btlDN.Scer\UAS, Scer\GAL4ato.3.6
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Scer\GAL460/Rac1Scer\UAS.cLa is a non-enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
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Rac1Scer\UAS.cLa, Scer\GAL4ato.3.6 is a suppressor of axon & dorsal cluster neuron & adult brain phenotype of Scer\GAL4ato.3.6, btlDN.Scer\UAS
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Expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[sns.PK] does not rescue myoblast fusion in homozygous mbc[D11.2] embryos.
The ISNb bypass phenotype of N[l1N-ts1] mutant embryos is not significantly modulated by expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[60].
A dar1[3010] mutant background does not block the dendrite branching activity found upon expression of Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[477].
One copy of trio[S137203] partially suppresses the larval neuromuscular junction overgrowth and bouton number phenotypes seen when Rac1[Scer\UAS.cLa] is expressed in neurons under the control of Scer\GAL4[OK6]. Bouton number is reduced by more than 50%. One copy of sif[ES11] is unable to suppress the increase in larval neuromuscular junction bouton number seen when Rac1[Scer\UAS.cLa] is expressed in neurons under the control of Scer\GAL4[OK6]. Homozygous trio[S137203] suppresses the larval neuromuscular junction overgrowth and increase in bouton number seen when Rac1[Scer\UAS.cLa] is expressed in neurons under the control of Scer\GAL4[OK6]. wit[A12]/wit[HA3] suppresses the increase in evoked excitatory junctional potential (EJPs) and quantal content seen when Rac1[Scer\UAS.cLa] is expressed in motor neurons under the control of Scer\GAL4[BG380], with third instar larvae instead displaying the reduction in neurotransmitter release phenotype seen in wit[A12]/wit[HA3] mutants. trio[S137203]/trio[6A] suppresses the increase in evoked excitatory junctional potential (EJPs) and quantal content seen when Rac1[Scer\UAS.cLa] is expressed in neurons under the control of Scer\GAL4[OK6].
Co-expression of Rac1[Scer\UAS.cLa] enhances the partial rescue of pbl[3] mesodermal migration defects seen when pbl[ΔBRCT.Scer\UAS.T:Hsap\MYC] is expressed under the control of Scer\GAL4[twi.2PE]. Co-expression of Rac1[Scer\UAS.cLa] strongly enhances the eye phenotype seen when pbl[DH-PH.Scer\UAS.T:Ivir\HA1] is expressed under the control of Scer\GAL4[GMR.PU]. Most flies die as pharate adults but escapers fail to develop any eye structures.
Ectopic expression of Rac1[Scer\UAS.cLa] along with ct[Scer\UAS.cPa] in class I neurons under the control of Scer\GAL4[221] leads to the formation of an arbor with many filpodia/spikes, which shows a significant enhancement of branching as compared to either Rac1[Scer\UAS.cLa] or ct[Scer\UAS.cPa] expression alone. Ectopic expression of Rac1[Scer\UAS.cLa] along with kn[Scer\UAS.cMa] in class I neurons under the control of Scer\GAL4[221] promotes the outgrowth of bona fide dendrites from the thorn-shaped projections initiated by Rac1[Scer\UAS.cLa] expression. In addition, coexpression of kn[Scer\UAS.cMa] causes a small, significant reduction in termini number.
Coexpression of Rac1Scer\UAS.cLa and btlDN.Scer\UAS, under the control of Scer\GAL4ato.3.6, results in the dominance of the Rac1Scer\UAS.cLa phenotype, with a reduction in the number of dorsal cluster neuron axons crossing toward the medulla. This indicates that the Rac1N17.Scer\UAS phenotype is dominant.
the addition of Rac1Scer\UAS.cLa to plexBScer\UAS.cHa, Scer\GAL4elav.PLu flies suppresses the Intersegmental nerve and RP3 nerve phenotypes.
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The viability of flies expressing Rac1[Scer\UAS.cLa] under the control of Scer\GAL4[GMR.PF] is enhanced to 50% by co-expression of Zzzz\ExoS[GAP.Scer\UAS]. In addition, the eye morphology of the surviving adults is restored towards wild type.
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Partially rescues
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.
The border follicle cell migration defect seen in egg chambers expressing Rac1N17.Scer\UAS under the control of Scer\GAL4slbo.2.6 is partially suppressed by coexpression of Rac1Scer\UAS.cLa.
Restores CNS pathways to near normal morphology, some abnormalities can be seen in occasional segments.
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Bloomington
Kyoto
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Reported As
Symbol Synonym
Rac1Scer\UAS.cLa
 
Rac1UAS.cLa
 
Name Synonym
Saccharomyces cerevisiae UAS construct of Luo
Secondary FlyBase IDs
hide References ( 28 )
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hide Recent research papers ( 5 )
Nagel et al., 2012, Development 139(16): 2999--3009
Fascin controls neuronal class-specific dendrite arbor morphology. [FBrf0219030]
Tsubouchi et al., 2012, Curr. Biol. 22(22): 2124--2134
Dendritic Filopodia, Ripped Pocket, NOMPC, and NMDARs Contribute to the Sense of Touch in Drosophila Larvae. [FBrf0219946]
Haralalka et al., 2011, Development 138(8): 1551--1562
Asymmetric Mbc, active Rac1 and F-actin foci in the fusion-competent myoblasts during myoblast fusion in Drosophila. [FBrf0213340]
Song and Giniger, 2011, Dev. Dyn. 240(2): 324--332
Noncanonical notch function in motor axon guidance is mediated by Rac GTPase and the GEF1 domain of trio. [FBrf0212819]
Ye et al., 2011, J. Neurosci. 31(9): 3309--3319
Differential regulation of dendritic and axonal development by the novel kruppel-like factor dar1. [FBrf0213162]
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