|Feature type||allele||Associated gene||Dmel\Cdc42|
|Also Known As||Cdc42V12|
|Allele class||gain of function allele|
|Mutagen||in vitro construct - regulatory fusion, in vitro construct - amino acid replacement|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Construct: Amino acid replacement: G12V. Scer\UAS sequences drive expression of a mutated form of Cdc42.
A constitutively active form of Cdc42 is expressed under the control of Scer\UAS regulatory sequences.
|Carried in construct|
(Medioni and Noselli, 2005, Sanchez-Soriano et al., 2005, Kaufmann et al., 1998, Sepp and Auld, 2003, Harden et al., 2002, Magie et al., 2002, Schneeberger and Raabe, 2003, Lawrence et al., 2002, Fritz and VanBerkum, 2002, Kunwar et al., 2003, Brumby and Richardson, 2003, Jhaveri et al., 2004, Baron et al., 2000, Chang and Ready, 2000, Luo et al., 1994, Jacobs et al., 2000, Benlali et al., 2000, Agnes et al., 1999, Szuts and Bienz, 2000, Martin-Bermudo et al., 1999, Gao et al., 1999, Harden et al., 1999, Ricos et al., 1999, Wilson et al., 2005, Sotillos and Campuzano, 2000, Conder et al., 2004, Murphy and Montell, 1996, Eaton et al., 1995, Dobens et al., 2001, Glise and Noselli, 1997, Sone et al., 1997, Hutterer et al., 2004, Srahna et al., 2006, Dorsten et al., 2007, Blanke and Jackle, 2006, Wolf et al., 2002, Kim et al., 2002, Allen et al., 2000, Paladi and Tepass, 2004, Schafer et al., 2007, Atwood et al., 2007, Song and Giniger, 2011, Nahm et al., 2010, Sem et al., 2002, Sampson et al., 2012, Fletcher et al., 2012, Jean et al., 2012, Taniguchi et al., 2007)
|Phenotype Manifest In|
tergal depressor of trochanter muscle motor neuron & dendrite, with Scer\GAL4shakB.lethal.4.1
Primary macrophages isolated from animals expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[Cg.PA] have an similar number of F-actin rich protrusions to wild type.
Expression of Cdc42[V12.Scer\UAS] in the muscles driven by Scer\GAL4[Mhc.Switch.PO] in the absence of RU486 is sufficient to decrease all parameters of synaptic growth.
Mitotic neuroblasts expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[pros.PMG] display normal cell polarity. Expression of Cdc42[V12.Scer\UAS] in neuroblasts from their formation, under the control of Scer\GAL4[wor.PA], results in a dramatic increase in the number of neuroblasts with cell polarity defects.
Stage 16 embryos overexpressing Cdc42[V12.Scer\UAS] driven by Scer\GAL4[ftz.ng] display axon bundles that cross the midline inappropriately.
Expression of Cdc42[V12.Scer\UAS] in the developing mesoderm under the control of Scer\GAL4[twi.PG] does not affect myoblast fusion although these embryos do show muscle attachment defects.
Expression of Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[Gap1-NP3392] results in defects in the left-right asymmetry of the anterior midgut. 13% of embryos show inversion of the normal left-right asymmetry.
Expression of Cdc42V12.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.
Dendrites of aCC and RP2 neurons expressing Cdc42V12.Scer\UAS under the control of Scer\GAL4eve.RN2 are irregular and shorter than wild-type dendrites. Scer\GAL4eve.RN2 > Cdc42V12.Scer\UAS-expressing RP2 neurons have a tendency of soma displacement from the CNS midline to positions lateral of the neuropile. The primary neurites project straight into the peripheral nerve without contacting the neuropile and without budding off dendrites. Dendrites of lateralised RP2 neurons are formed in the correct position of the neuropile but emanate from the region of their cell bodies that is closest to the dorsal neuropile, instead of from primary neurites.
The antennal lobes of Cdc42V12.Scer\UAS; Scer\GAL4SG18.1 flies lack discernible glomeruli. Instead there are a clear glomerular-like structures within the antennal commissure where axons ectopically terminate.
Expression of Cdc42[V12.Scer\UAS] under the control of either Scer\GAL4[Cg25C-A109.1F2.P] or Scer\GAL4[gcm-rA87.P] does not interfere with the migration or distribution of macrophages in the embryo. Macrophages have only short cytoplasmic protrusions in embryos expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[Cg25C-A109.1F2.P] and have a rounded morphology. Embryos expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[gcm-rA87.P] have a reduced number of larger than normal macrophages compared to wild-type controls. The macrophages have wild-type cytoplasmic protrusions and normal F-actin content. A fraction of the macrophages are binucleate.
Cdc42N17.Scer\UAS when driven by Scer\GAL4nos.UTR.T:Hsim\VP16 has no effect on transepithelial migration of germ cells in the embryo.
Cdc42V12.Scer\UAS driven by Scer\GAL4repo has no effect on the glia of the peripheral nervous system.
When Cdc42V12.Scer\UAS is driven by Scer\GAL4ftz.ng, midline crossovers are seen in the pCC/MP2 pathway axons in 88% of embryos. An average of 3.6 crossovers are seen per embryo. When Cdc42V12.Scer\UAS is driven by Scer\GAL4elav.PLu, no adults eclose.
Expression of Cdc42V12.Scer\UAS driven by Scer\GAL4332.3 does not affect either the dorsal cuticle or amnioserosa morphology.
Expression of Cdc42[V12.Scer\UAS] in neurons under the control of either Scer\GAL4[elav-C155] or Scer\GAL4[elav.PLu] results in motor axons exhibiting navigation patterns ranging from virtually normal to clearly abnormal. The frequency of abnormalities in each group is higher with Scer\GAL4[elav.PLu] than with Scer\GAL4[elav-C155]. SNb axons expressing Scer\GAL4[elav-C155]-driven Cdc42[V12.Scer\UAS] display abnormal pathfinding patterns in 84% of cases. Their phenotypes are categorized as: turning posteriorly in unision at an incorret site, i.e. muscle 7, 15, or 16 (25%); stalling at or before muscle 6 (40%); or absence in the ventral musculature attributable presumably to either stalling within the CNS or bypassing the SNb pathway after leaving the CNS (19%). Abnormal turning as early as hour 12 (stage 14), when these axons in wild-type would be navigating around muscles 15 and 16 and beginning to contact the more distal muscles 6 and 7, is also found. When a high-expression Scer\GAL4[elav.PLu] driver is used, the most common phenotype of SNb axons shifts from abnormal turning to a complete absence in the ventral musculature, although there are still cases (9%) in which SNb axons display abnormal turn at muscle 15 or 16. SNd axons expressing Scer\GAL4[elav-C155]-driven Cdc42[V12.Scer\UAS] display abnormal pathfinding patterns in 47% of cases. SNa axon pathfinding is affected in 5% of cases, while SNc axon pathfinding is affected in 2% of cases. SNd axons expressing Scer\GAL4[elav.PLu]-driven Cdc42[V12.Scer\UAS] display abnormal pathfinding patterns in 100% of cases. SNa axon pathfinding is affected in 66% of cases, while SNc axon pathfinding is affected in 39% of cases. Expression of Cdc42[V12.Scer\UAS] in neurons under the control of Scer\GAL4[elav.PLu] or Scer\GAL4[elav-C155] has little effect on LBD neuron pathfinding. Mutant LBD axons do not navigate at a speed different from wild-type controls. Expression of Cdc42[V12.Scer\UAS] in neurons under the control of Scer\GAL4[elav-C155] results in an increase in filopodial extension and retraction rates by 52%, and the filopodia length increases by 38%. Similarly, expression under the control of Scer\GAL4[elav.PLu] results in a 51% increase in filopodia length and 31% and 38% increases, respectively, in extension and retraction rates. SNb growth cones at hour 12-14 expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[elav-C155] consistently deviate from the wild-type pathway, directing their growth cones toward muscles 15 and 16. SNb axons are directed posteriorly at angles greater than -20[o] compared to wild-type, which maintains growth cone angles of approximately 4.7[o]. Despite this, filopodial extension and retraction rates are similar to those of wild-type controls, and the length of filopodia increases by 5%. There is no significant difference in either the number or longevity of individual filopodia directed posteriorly versus anteriorly.
Ectopic cellular extensions are seen in the tracheal cells of stage 12 embryos expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[btl.PS].
Scer\GAL4[A307]; Cdc42[V12.Scer\UAS] flies are viable at 25[o]C. Adult flies exhibit no neurite extension. The GF cell bodies can be observed, but no dendritic field or axons can be found. No muscle responses are found when thoracic stimulation is used to directly activate the motor neurons. Scer\GAL4[c17]; Cdc42[V12.Scer\UAS] adult GFs show no neurite outgrowth. These flies show no responses upon brain stimulation. However, upon thoracic stimulation of the same fly, to activate the motor neurons directly, the fast response latencies are seen in both the TTM and the DLM and both have following frequencies of 100% at 250Hz.
When Cdc42V12.Scer\UAS is driven by Scer\GAL4Bx-MS1096, viable adults with a strong macrochaetae and microchaetae loss phenotype on the notum are produced. The wings on these animals are residual stumps.
Expression of Cdc42V12.Scer\UAS under the control of Scer\GAL4ey.PH results in an extreme reduction in the size of the eye disc.
The tergotrochanteral muscle motorneuron cell bodies are present in flies expressing Cdc42V12.Scer\UAS under the control of Scer\GAL4shakB.lethal.4.1, but medial dendrites are much reduced or absent. The Giant Fibre (GF) always lacks its normal bend in these flies. Fine processes are seen emanating from the distal tip of the GF, which often project laterally or extend towards the metathoracic neuromere.
When expression is driven by Scer\GAL4dpp.blk1 aberrant and premature fusion of the mesothoracic ventral thoracic discs frequently occurs in L3 larvae.
When driven in postmitotic neurons by Scer\GAL460, Cdc42V12.Scer\UAS promotes primary dendrite outgrowth and inhibits secondary lateral branching. Dorsal primary branches from md neurons fail to fully extend and appear abnormally thick, multiple dorsal dendrites extend from the neuron where there would be only one in wild-type. The number of lateral secondary branches is also reduced.
Most of the cuticles of embryos expressing Cdc42V12.Scer\UAS under the control of Scer\GAL4ptc-559.1 are distorted or missing. Embryos expressing Cdc42V12.Scer\UAS under the control of Scer\GAL4hs.PB (using heat shock) have a high frequency of puckers in the dorsal surface.
Expression of Cdc42V12.Scer\UAS under the control of Scer\GAL448Y in the developing midgut does not result in accelerated migration of the endodermal midgut cells.
Scer\GAL4elav.PLu-mediated expression causes arrest of late ISNb growth cone at contact with muscle 13.
When driven by a Scer\GAL4 line expressed under the influence of an elav promoter, the SNb motor neuron bundle is missing.
Spontaneous and evoked muscle contraction with Scer\GAL4how-24B, little muscle contraction with Scer\GAL41407. With Scer\GAL41407 the dorsal clusters are shorter and rounder, there is some axonal loss between the lateral and dorsal clusters and the dendrites are abnormal or absent. In the presence of Scer\GAL4how-24B a small number of larvae hatch that exhibit abnormal morphology of muscle fibres.
|NOT Enhancer of|
|Phenotype Manifest In|
|NOT Enhanced by|
Cdc42V12.Scer\UAS, Scer\GAL4ftz.ng has midline crossing tract | embryonic stage 16 phenotype, suppressible | partially by fra4/fra[+]
Cdc42V12.Scer\UAS, Scer\GAL4ftz.ng has ventral nerve cord commissure | embryonic stage 16 phenotype, suppressible | partially by fra4/fra[+]
|NOT suppressed by|
Cdc42V12.Scer\UAS, Scer\GAL4ftz.ng is an enhancer of dMP2 neuron phenotype of Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng
Cdc42V12.Scer\UAS, Scer\GAL4ftz.ng is an enhancer of pCC neuron phenotype of Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng
Cdc42V12.Scer\UAS, Scer\GAL4ftz.ng is an enhancer of vMP2 neuron phenotype of Ggal\MLCKct.Scer\UAS, Scer\GAL4ftz.ng
|NOT Enhancer of|
Scer\GAL460/Cdc42V12.Scer\UAS is a non-enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
Scer\GAL460/Cdc42V12.Scer\UAS is a non-enhancer of intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of Nl1N-ts1
Scer\GAL4btl.PS/Cdc42V12.Scer\UAS is a suppressor | partially of embryonic/larval dorsal trunk phenotype of bnl00857
|NOT Suppressor of|
Cdc42V12.Scer\UAS, Rac1N17.hs, Scer\GAL4hs.PB has embryonic/first instar larval cuticle | dorsal phenotype
Expression of Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[He.PZ] rescues the reduced rate of encapsulation of eggs of the avirulent wasp strain L. boulardi G486 that is seen in Zir[BG00267] larvae. Expression of Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[He.PZ] rescues the reduced phagocytosis index against E. coli and S. aureus seen in isolated plasmatocytes from homozygous Zir[BG00267] larvae.
The ISNb bypass phenotype of N[l1N-ts1] mutant embryos is not significantly modulated by expression of Cdc42[V12.Scer\UAS] (under the control of Scer\GAL4).
Heterozygous fra partially suppresses the incorrect midline crossing phenotype of ventral nerve cord axons in embryos overexpressing Cdc42[V12.Scer\UAS] via Scer\GAL4[ftz.ng].
puc[GS16811]/+ has no effect on the defects in left-right asymmetry of the anterior midgut which are seen in embryos expressing Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[Gap1-NP3392].
The addition of Cdc42V12.Scer\UAS (driven by Scer\GAL4ftz.ng) to robo1/+ embryos has no effect on the midline crossover phenotype seen in the pCC/MP2 pathway axons. The addition of Cdc42V12.Scer\UAS (driven by Scer\GAL4ftz.ng) to Sose49 homozygous embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. All embryos exhibit the phenotype. The addition of chicsand-1 to Cdc42V12.Scer\UAS suppresses the midline crossover phenotypes in the pCC/MP2 pathway axons. 45.5% of embryos exhibit the phenotype. An average of 1.9 crossovers are seen per embryo.
Expression of Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[btl.PS] in a bnl background show occasional (4.4%) fusions of the adjacent lollipop-like dorsal trunk structures (bnl single mutants show no fusion of the adjacent metameric tracheal units).
When Rac1N17.hs is co-expressed with Cdc42V12.Scer\UAS under the control of Scer\GAL4hs.PB most cuticles are extremely disrupted. There is evidence of some rescue of the Rac1N17.hs phenotype by Cdc42V12.Scer\UAS expressed under the control of Scer\GAL4hs.PB, as there are greater numbers of wild-type and mild dorsal closure defective embryos than seen with the expression of Rac1N17.hs alone.
|Complementation & Rescue Data|
|Stocks ( 4 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 49 )|
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|Recent research papers ( 4 )|
|Recent reviews (0)|
|All reviews listed in FlyBase were published before 2011|