Open Close
General Information
Symbol
Dmel\Cdc42N17.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0038150
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Cdc42N17, Cdc42N17, UAS-Dcdc42N17, UAS-Dcdc42N17, cdc42-DN, UAS-cdc42N17, Cdc42N17
Nature of the Allele
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

UAS sequences drive expression of a mutated form of Cdc42 (carries the amino acid replacement T17N).

UASt regulatory sequences drive expression of a dominant-negative form of Cdc42.

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 ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

antenna & glial cell, with Scer\GAL4Mz317

antenna & sensory neuron, with Scer\GAL4Mz317

embryonic hemocyte & leading edge, with Scer\GAL4Pxn.PS, Scer\GAL4crq.PA

Detailed Description
Statement
Reference

The expression of Cdc42N17.UAS under the control of Scer\GAL4da.G32 leads to severe cuticle defects in the embryo.

Scer\GAL4btl.PS-mediated expression of Cdc42N17.Scer\UAS causes tracheal lateral trunk fusion defects.

Class III ddaA neurons expressing Cdc42N17.Scer\UAS under the control of Scer\GAL41003.3 show a significant decrease in the number of dendritic sensory filopodia compared to wild type. The average length of the filopodia is significantly increased compared to wild type, while the total length of primary dendritic branches is not altered.

Larvae expressing Cdc42N17.Scer\UAS under the control of Scer\GAL41003.3 show a reduced response to gentle touch compared to controls.

Flies expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4tin.CΔ4 (in combination with GAL80 to restrict the expression to the first week of adult life) exhibit a significantly increased pacing-induced heart failure rate, increased incidence of arrhythmias, overall lower heart rates due to longer diastolic intervals, severely misaligned myofibrils, and irregularities in the Z-line pattern of the cardiomyocytes, as compared with controls. Systolic intervals are not significantly changed in these flies.

Flies expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4how-24B (in combination with GAL80 to restrict the expression to the first week of adult life) exhibit a significantly increased pacing-induced heart failure rate, increased incidence of arrhythmias, severely misaligned myofibrils, and irregularities in the Z-line pattern of the cardiomyocytes, as compared with controls. Systolic intervals are not significantly changed in these flies.

Expression of Cdc42N17.Scer\UAS in the muscles driven by Scer\GAL4Mhc.Switch.PO in the absence of RU486 is sufficient to decrease all parameters of synaptic growth.

Expression of Cdc42N17.Scer\UAS under the control of either Scer\GAL4elav.PU or Scer\GAL4ey-OK107 (using tub-Gal80[ts] to limit the expression to the adult stage) significantly improves 3 hr memory of adult flies in an aversive olfactory assay compared to controls.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4en-e16E results in a strong multiple wing hair phenotype.

Mitotic neuroblasts expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4pros.PMG display normal cell polarity. Expression of Cdc42N17.Scer\UAS in neuroblasts from their formation, under the control of Scer\GAL4wor.PA, results in a dramatic increase in the number of neuroblasts with cell polarity defects.

Scer\GAL4en-e16E-mediated expression of Cdc42N17.Scer\UAS causes duplications of crossveins.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4ato.3.6 does not affect dorsal cluster neuron axon extension across the optic chiasm in adult flies.

Expression of Cdc42N17.Scer\UAS in border cells, driven by Scer\GAL4slbo.2.6 does not affect the formation of the egg chamber apical cap or the migration of the border cell cluster to the oocyte.

Hemocytes in embryos expressing Cdc42N17.Scer\UAS under the simultaneous control of both Scer\GAL4Pxn.PS and Scer\GAL4crq.PA show normal developmental dispersal and normal recruitment to sites of laser-induced tissue damage. However, during the migratory phase and after arrival at the wound site, the mutant hemocytes often possess several leading edges suggesting that they cannot maintain a persistent polarity.

The failure of hemocytes to maintain polarity in embryos expressing Cdc42N17.Scer\UAS under the simultaneous control of both Scer\GAL4Pxn.PS and Scer\GAL4crq.PA leads them to adopt a haphazard migratory route. This defect is countered by the mutant hemocytes migrating at approximately twice the normal speed so that they reach the wound as rapidly as in wild type embryos.

Expression of Cdc42N17.Scer\UAS in the muscle, under the regulation of Scer\GAL4Mhc.PW has no effect on synapse development.

In Cdc42N17.Scer\UAS; Scer\GAL4retn-GAL4 embryos, invagination of the ectodermal keyhole cells during development of the proventriculus is defective.

Expression of Cdc42N17.Scer\UAS under the control of either Scer\GAL4Cg25C-A109.1F2.P or Scer\GAL4gcm-rA87.P does not interfere with the migration or distribution of macrophages in the embryo.

Macrophages have wild-type cytoplasmic protrusions and normal F-actin content in embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4gcm-rA87.P. Macrophages have wild-type morphology in embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4Cg25C-A109.1F2.P.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4da.G32 causes defects in macrophage migration in the embryo.

When Cdc42N17.Scer\UAS is overexpressed, mutants do not exhibit longitudinal axon ectopic midline crossing defects.

Cdc42N17.Scer\UAS when driven by Scer\GAL4nos.UTR.T:Hsim\VP16 has no effect on transepithelial migration of germ cells in the embryo.

Cdc42N17.Scer\UAS driven by Scer\GAL4repo has no effect on the glia of the peripheral nervous system.

When Cdc42N17.Scer\UAS is driven by Scer\GAL4ftz.ng, no midline crossovers are seen in the pCC/MP2 pathway axons. When Cdc42N17.Scer\UAS is driven by Scer\GAL4elav.PLu only half of the expected number of adults eclose.

Expression of Cdc42N17.Scer\UAS driven by Scer\GAL4332.3 does not affect either the dorsal cuticle or amnioserosa morphology.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4Mz317 results in a reduction in the number of glial cells in the antenna, and the residual glial cells are aggregated with no apparent processes. Sensory neurons in the antenna show a number of defects in fasciculation. The antennal glomeruli in the olfactory lobe develop normally in these animals and there are no defects in the lobe-associated glia or their extensions into the lobe.

Expression of dominant-negative Cdc42N17.Scer\UAS in SNb neurons under the control of Scer\GAL4elav-C155 results in abnormal pathfinding patterns in 15% of cases.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4btl.PS does not affect lumen formation in the tracheal system although these embryos do show some defects in tracheal branch migration.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB using heat shock results in a failure of dorsal closure in the embryo, producing dorsal holes in the cuticle.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.2sev using heat shock results in breaks in the tracheal dorsal trunk in embryos in 32% of cases.

Cdc42N17.Scer\UAS; Scer\GAL4en-e16E embryos complete dorsal closure but fail to survive to larval stages. In these embryos, small laser wounds (approximately 2 cell diameters in width) assemble an actin cable in leading-edge cells at the same rate as in wild-type. However, no filopodial or lamellipodial protrusions extend from any of the leading-edge cells throughout wound closure. At 30 min after wounding, the hole is almost closed but, unlike wild-type epithelium, which undergoes this final closure phase in less than 15 min, the hole remains unsealed even 2 hours after wounding.

Co-expression of Cdc42N17.Scer\UAS has little or no effect on the gain of function axon guidance defects caused by expression of Gef64CEP3035 under the control of Scer\GAL4elav.PLu.

Cells expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4Act5C.PP in large clones in the posterior follicle cells delaminate and leave the continuous follicle epithelium.

Embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4ptc-559.1 have a dorsal hole.

Eggs derived from females expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4CY2 have thinner dorsal appendages than normal which are irregular in shape.

Cdc42N17.Scer\UAS when driven by Scer\GAL4Bx-MS1096, results in a strong multiple wing hair phenotype, a reduction in wing size, ectopic vein tissue and wing margin phenotypes. In the wing margin, expression causes a reduction of bristle density with the stout mechanosensors being most affected; in many wings these are completely absent. However the remaining margin occupies a broader area than normal. When driven by Scer\GAL4ptc-559.1, a non-autonomous ectopic crossvein phenotype is seen.

When Cdc42N17.Scer\UAS is driven by Scer\GAL4en-e16E in embryos at the zippering stage, just before dorsal closure, the normal extension of actin based filopodia and lamellae is not seen at the dorsal holes edge. A severe failure to seam and a misalignment of the seamed edges is also seen in these embryos.

Embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4ptc-559.1 show a high frequency of dorsal cuticle defects, with most embryos having a large hole towards the posterior of the embryo. Embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB (using heat shock) can survive to the first larval instar stage depending on the Scer\GAL4hs.PB line used. Phenotypes include a mild puckering of the cuticle with very few dorsal holes, dorsal holes in the cuticle and embryos having at least one or usually several instances of the dorsal ends of segments being pulled together at the leading edge into bunches.

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL448Y in the developing midgut causes a delay in migration of the endodermal midgut cells.

Embryos expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB show bunching of epidermal segments at the end of dorsal closure.

Scer\GAL4twi.PG-mediated expression causes severe cuticle defects.

Scer\GAL4-mediated expression fails to cause any defects.

When expression is driven by Scer\GAL469B the embryos show a dorsal open phenotype.

Semi-embryonic lethal with Scer\GAL41407, some individuals survive to adulthood.

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

Scer\GAL4elav-C155/Cdc42N17.UAS is a non-enhancer of neuroanatomy defective | heat sensitive phenotype of Nl1N-ts1

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Statement
Reference
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4ey.PH rescues the glossy eye phenotype seen in btlLG19 mutant clones.

The ISNb bypass phenotype of Nl1N-ts1 mutant embryos is not significantly modulated by expression of Cdc42N17.Scer\UAS (under the control of Scer\GAL4elav-C155).

Expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4NP2225 does not suppress the reduction in length of secondary dendritic branches which is seen in the ddaE neurons of cv-c1260 embryos at 20-22 hours after egg laying.

When Cdc42N17.Scer\UAS is added to RhoGAP93BScer\UAS.cHa, Scer\GAL4elav.PLu embryos, no enhancement of the ectopic midline crossing phenotype is seen in the ventral nerve cord.

Co-expression of Cdc42N17.Scer\UAS and Rac1N17.Scer\UAS in the muscle, under the regulation of Scer\GAL4Mhc.PW has no effect on gross synapse development.

The combination of heterozygous sli2 and pan-neural overexpression of Cdc42N17.Scer\UAS (expressed under the control of Scer\GAL4elav.PLu) does not cause longitudinal axon ectopic midline crossing defects.

The addition of Cdc42N17.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 18% of embryos exhibit the phenotype. An average of 1.2 crossovers are seen per embryo. The addition of Cdc42N17.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49/+ embryos has no effect on the midline crossover phenotype seen in the pCC/MP2 pathway axons. The addition of chicsand-1 to Cdc42N17.Scer\UAS has no effect on their midline crossover phenotypes in the pCC/MP2 pathway axons.

Co-expression of AckScer\UAS.cSa partially suppresses the dorsal closure defects caused by expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB using heat shock.

The loss of one copy of N by the addition of Df(1)N-54l9 to Cdc42N17.Scer\UAS, Scer\GAL4Bx-MS1096 flies restores the stout mechanosensor bristle phenotype. The addition of NAx-E2 enhances the wing margin phenotype.

The dorsal closure defects of embryos co-expressing Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 4 to 8 hours after egg laying are more severe than the defects produced by expression of either Rac1N17.hs or Cdc42N17.Scer\UAS alone. In contrast, the defects produced by co-expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB and Rac1N17.hs (using heat shock) 8 to 12 hours after egg laying are weaker than Rac1N17.hs expressed alone, but stronger than Cdc42N17.Scer\UAS expressed alone.

tkvTAJ3 has no effect on the phenotype caused by expression of Cdc42N17.Scer\UAS under the control of Scer\GAL4hs.PB.

Xenogenetic Interactions
Statement
Reference

The addition of Cdc42N17.Scer\UAS to Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng embryos partially suppresses the midline crossover phenotype seen in the pCC/MP2 pathway axons. 4.4% of embryos exhibit the phenotype. An average of 1.3 crossovers are seen per embryo.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
  • FBal0038149
References (61)