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General Information
Symbol
Dmel\Rac1UAS.cLa
Species
D. melanogaster
Name
Saccharomyces cerevisiae UAS construct of Luo
FlyBase ID
FBal0038995
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rac1, UAS-rac, UAS-DRac1, UAS-rac1.L
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of a Rac1 cDNA.

Allele components
Product class / Tool use(s)
Encoded product / tool
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 ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

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

Detailed Description
Statement
Reference

Scer\GAL4ppk.PG-mediated overexpression of Rac1Scer\UAS.cLa drives ectopic dendrite branching, although total dendrite length is unaffected. This increase in terminal dendrite branching is accompanied by a significant decrease in primary dendrite growth - as a result, distal portions of the territory normally covered by C4da neurons are completely devoid of dendrites.

Expression of Rac1Scer\UAS.cLa for 12 hours under the control of Scer\GAL4P0.5.Pdf (restricted to the adult stages using Scer\GAL80ts.αTub84B) significantly increases the spread of s-LNv projections in the x and y axes at dawn (ZT24).

Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4P0.5.Pdf lengthens the behavioral rhythm period to 25 hours.

Overexpressing Rac1Scer\UAS.cLa in class IV da neurons (Scer\GAL4ppk.PU) partially (increased regeneration percentage but not terminal branching or commissure growth) improves axon regeneration.

Overexpression of Rac1Scer\UAS.cLa driven by Scer\GAL4109(2)80 leads to a significant increase in dendrite branch points (but not length) in class I da sensory neurons compared to wild type.

Class III ddaA neurons expressing Rac1Scer\UAS.cLa under the control of Scer\GAL41003.3 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 Rac1Scer\UAS.cLa under the control of Scer\GAL41003.3 are hypersensitive to gentle touch compared to controls.

Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4ppk.PG promotes F-actin structure formation in the distal dendrites of dorsal cluster neurons.

Overexpression of Rac1Scer\UAS.cLa in many neuron types, including the da neurons, under the control of Scer\GAL4477, leads to hyperbranching of dendrites.

Expression of Rac1Scer\UAS.cLa under the control of the neuronal drivers Scer\GAL4BG380, Scer\GAL4OK6 or Scer\GAL4elav-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 Rac1Scer\UAS.cLa is expressed in muscle under the control of the Scer\GAL4Mhc.PW driver.

Expression of Rac1Scer\UAS.cLa under the control of either Scer\GAL4BG380 or Scer\GAL4OK6 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 Rac1Scer\UAS.cLa under the control of Scer\GAL4DB331 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 Rac1Scer\UAS.cLa under the control of Scer\GAL4221 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 Rac1Scer\UAS.cLa under the control of Scer\GAL4GMR.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 Rac1Scer\UAS.cLa to the GF under the control of Scer\GAL4A307 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\GAL4A307; Rac1Scer\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\GAL4A307; Rac1Scer\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\GAL4c17; Rac1Scer\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\GAL4A307; Rac1Scer\UAS.cLa flies exhibit a bendless GF phenotype, while 64% of Scer\GAL4A307; Rac1Scer\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.

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

Scer\GAL460/Rac1UAS.cLa is a non-enhancer of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1

Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference

Rac1UAS.cLa, Scer\GAL4ato.3.6 has axon & dorsal cluster neuron phenotype, non-enhanceable by btlDN.UAS, Scer\GAL4ato.3.6

Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference

Scer\GAL460/Rac1UAS.cLa is a non-enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Suppressor of
Statement
Reference

Rac1UAS.cLa, Scer\GAL4ato.3.6 is a suppressor of axon & dorsal cluster neuron & adult brain phenotype of Scer\GAL4ato.3.6, btlDN.UAS

NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Expression of PuraGD12260 does not suppress the increase in length of the behavioral rhythm period seen when Rac1Scer\UAS.cLa is expressed under the control of Scer\GAL4P0.5.Pdf.

Expression of Rac1Scer\UAS.cLa driven by Scer\GAL4109(2)80 partially suppresses the reduction of dendritic spikes seen in class III da sensory neuron fs(1)h1112/fs(1)h1112 larval clones.

Loss of fs(1)h1112/fs(1)h1112 in class I da neuron clones does not suppress the increase in dendrite branch points seen in larvae with Rac1Scer\UAS.cLa overexpression driven by Scer\GAL4109(2)80.

Co-expression of Rac1Scer\UAS.cLa suppresses the decrease in zippering speed during dorsal closure seen in cells expressing PtenScer\UAS.cGa under the control of Scer\GAL4en.PU. The reduction in number of filopodia at the leading edge is also suppressed.

Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4sns.PK does not rescue myoblast fusion in homozygous mbcD11.2 embryos.

The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Rac1Scer\UAS.cLa under the control of Scer\GAL460.

A dar13010 mutant background does not block the dendrite branching activity found upon expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4477.

One copy of trioS137203 partially suppresses the larval neuromuscular junction overgrowth and bouton number phenotypes seen when Rac1Scer\UAS.cLa is expressed in neurons under the control of Scer\GAL4OK6. Bouton number is reduced by more than 50%.

One copy of sifES11 is unable to suppress the increase in larval neuromuscular junction bouton number seen when Rac1Scer\UAS.cLa is expressed in neurons under the control of Scer\GAL4OK6.

Homozygous trioS137203 suppresses the larval neuromuscular junction overgrowth and increase in bouton number seen when Rac1Scer\UAS.cLa is expressed in neurons under the control of Scer\GAL4OK6.

witA12/witHA3 suppresses the increase in evoked excitatory junctional potential (EJPs) and quantal content seen when Rac1Scer\UAS.cLa is expressed in motor neurons under the control of Scer\GAL4BG380, with third instar larvae instead displaying the reduction in neurotransmitter release phenotype seen in witA12/witHA3 mutants.

trioS137203/trio6A suppresses the increase in evoked excitatory junctional potential (EJPs) and quantal content seen when Rac1Scer\UAS.cLa is expressed in neurons under the control of Scer\GAL4OK6.

Co-expression of Rac1Scer\UAS.cLa enhances the partial rescue of pbl3 mesodermal migration defects seen when pblΔBRCT.Scer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4twi.2PE.

Co-expression of Rac1Scer\UAS.cLa strongly enhances the eye phenotype seen when pblDH-PH.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU. Most flies die as pharate adults but escapers fail to develop any eye structures.

Ectopic expression of Rac1Scer\UAS.cLa along with ctScer\UAS.cPa in class I neurons under the control of Scer\GAL4221 leads to the formation of an arbor with many filpodia/spikes, which shows a significant enhancement of branching as compared to either Rac1Scer\UAS.cLa or ctScer\UAS.cPa expression alone.

Ectopic expression of Rac1Scer\UAS.cLa along with knScer\UAS.cMa in class I neurons under the control of Scer\GAL4221 promotes the outgrowth of bona fide dendrites from the thorn-shaped projections initiated by Rac1Scer\UAS.cLa expression. In addition, coexpression of knScer\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.

Xenogenetic Interactions
Statement
Reference

Expression of Rac1Scer\UAS.cLa partially suppresses the dendrite defects seen in class IV da neurons expressing Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ppk.PG. The reduction in F-actin structures in the distal dendrites of dorsal cluster neurons when Hsap\ATXN3tr.Q78.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4109(2)80 is also partially rescued.

The viability of flies expressing Rac1Scer\UAS.cLa under the control of Scer\GAL4GMR.PF is enhanced to 50% by co-expression of Zzzz\ExoSGAP.Scer\UAS. In addition, the eye morphology of the surviving adults is restored towards wild type.

Complementation and Rescue Data
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.

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.

Images (0)
Mutant
Wild-type
Stocks (3)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
Rac1Scer\UAS.cLa
Rac1UAS.cLa
Name Synonyms
Saccharomyces cerevisiae UAS construct of Luo
Secondary FlyBase IDs
    References (39)