Allele Dmel\Cdc42^V12.Scer\UAS

General Information
Symbol	Dmel\Cdc42^V12.Scer\UAS	Species	D. melanogaster
Name		FlyBase ID	FBal0038153
Feature type	allele	Associated gene	Dmel\Cdc42
Also Known As	Cdc42^V12

Allele class	gain of function allele
Mutagen	in vitro construct - regulatory fusion, in vitro construct - amino acid replacement
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class	gain of function allele (Sanchez-Soriano et al., 2005)
Mutagen	in vitro construct - amino acid replacement (Schneeberger and Raabe, 2003) in vitro construct - regulatory fusion (Luo et al., 1994, Eaton et al., 1995, Schneeberger and Raabe, 2003)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Construct: Amino acid replacement: G12V. Scer\UAS sequences drive expression of a mutated form of Cdc42. (Schneeberger and Raabe, 2003) A constitutively active form of Cdc42 is expressed under the control of Scer\UAS regulatory sequences. (Eaton et al., 1995) Construct: A constitutively active form of Cdc42 is expressed under the control of Scer\UAS regulatory sequences. (Luo et al., 1994)
Carried in construct	P{UAS-Cdc42.V12} (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)
Cytology
Phenotypic Data
Phenotypic Class
	cell polarity defective, with Scer\GAL4^wor.PA (Atwood et al., 2007) lethal, with Scer\GAL4^198Y (Murphy and Montell, 1996) lethal, with Scer\GAL4^238Y (Schneeberger and Raabe, 2003) lethal, with Scer\GAL4^elav.PLu (Fritz and VanBerkum, 2002) lethal, with Scer\GAL4^hs.PB (Murphy and Montell, 1996) lethal \| embryonic stage, with Scer\GAL4^en-e16E (Blanke and Jackle, 2006) lethal \| embryonic stage, with Scer\GAL4^how-24B (Luo et al., 1994) lethal \| female, with Scer\GAL4³⁰⁶ (Murphy and Montell, 1996) neuroanatomy defective, with Scer\GAL4^A307 (Allen et al., 2000) neuroanatomy defective, with Scer\GAL4^elav.PLu (Kim et al., 2002) neuroanatomy defective, with Scer\GAL4^elav-C155 (Kim et al., 2002) neuroanatomy defective, with Scer\GAL4^{Mhc.Switch.PO} (Nahm et al., 2010) neuroanatomy defective \| embryonic stage 16, with Scer\GAL4^ftz.ng (Dorsten et al., 2007) neurophysiology defective, with Scer\GAL4^A307 (Allen et al., 2000) partially lethal - majority die, with Scer\GAL4²¹² (Murphy and Montell, 1996) viable, with Scer\GAL4⁴⁵⁸ (Murphy and Montell, 1996) viable \| heat sensitive (Allen et al., 2000)
Phenotype Manifest In
	abdominal intersegmental nerve (Luo et al., 1994) abdominal intersegmental nerve, with Scer\GAL4^elav.PLu (Kaufmann et al., 1998) abdominal segmental nerve, with Scer\GAL4^elav.PLu (Sone et al., 1997, Kim et al., 2002) abdominal segmental nerve, with Scer\GAL4^elav-C155 (Kim et al., 2002) aCC neuron & dendrite, with Scer\GAL4^eve.RN2 (Sanchez-Soriano et al., 2005) antennal commissure, with Scer\GAL4^SG18.1 (Jhaveri et al., 2004) antennal lobe glomerulus, with Scer\GAL4^SG18.1 (Jhaveri et al., 2004) anterior embryonic/larval midgut, with Scer\GAL4^Gap1-NP3392 (Taniguchi et al., 2007) bouton, with Scer\GAL4^{Mhc.Switch.PO} (Nahm et al., 2010) dendrite (Luo et al., 1994) dendrite, with Scer\GAL4^A307 (Allen et al., 2000) dendrite \| dorsal \| embryonic stage, with Scer\GAL4⁶⁰ (Gao et al., 1999) dMP2 neuron, with Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) dorsal abdominal cluster (Luo et al., 1994) dorsal multidendritic neuron & dendrite & embryo, with Scer\GAL4⁶⁰ (Gao et al., 1999) dorsal multidendritic neuron \| embryonic stage, with Scer\GAL4⁶⁰ (Gao et al., 1999) embryonic/first instar larval cuticle, with Scer\GAL4^ptc-559.1 (Harden et al., 1999) embryonic/first instar larval cuticle \| dorsal, with Scer\GAL4^hs.PB (Harden et al., 1999) eye disc, with Scer\GAL4^ey.PH (Benlali et al., 2000) giant axon, with Scer\GAL4^A307 (Allen et al., 2000) giant fiber neuron, with Scer\GAL4^{shakB.lethal.4.1} (Jacobs et al., 2000) glomerulus \| ectopic, with Scer\GAL4^SG18.1 (Jhaveri et al., 2004) growth cone, with Scer\GAL4^elav.PLu (Kim et al., 2002) growth cone, with Scer\GAL4^elav-C155 (Kim et al., 2002) macrochaeta & metathoracic laterotergite, with Scer\GAL4^Bx-MS1096 (Baron et al., 2000) macrophage, with Scer\GAL4^{Cg25C-A109.1F2.P} (Paladi and Tepass, 2004) macrophage, with Scer\GAL4^gcm-rA87.P (Paladi and Tepass, 2004) mesothoracic leg disc, with Scer\GAL4^dpp.blk1 (Agnes et al., 1999) microchaeta & metathoracic laterotergite, with Scer\GAL4^Bx-MS1096 (Baron et al., 2000) midline crossing tract \| embryonic stage 16, with Scer\GAL4^ftz.ng (Dorsten et al., 2007) motor neuron, with Scer\GAL4^elav.PLu (Kim et al., 2002) motor neuron, with Scer\GAL4^elav-C155 (Kim et al., 2002) muscle attachment site, with Scer\GAL4^twi.PG (Schafer et al., 2007) neurite, with Scer\GAL4^A307 (Allen et al., 2000) neuroblast \| embryonic stage, with Scer\GAL4^wor.PA (Atwood et al., 2007) neuromuscular junction, with Scer\GAL4^{Mhc.Switch.PO} (Nahm et al., 2010) pCC neuron, with Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) presumptive embryonic/larval peripheral nervous system \| dorsal, with Scer\GAL4⁶⁰ (Gao et al., 1999) presumptive embryonic/larval tracheal system, with Scer\GAL4^btl.PS (Wolf et al., 2002) RP2 motor neuron \| ectopic, with Scer\GAL4^eve.RN2 (Sanchez-Soriano et al., 2005) RP2 neuron & cell body, with Scer\GAL4^eve.RN2 (Sanchez-Soriano et al., 2005) RP2 neuron & dendrite, with Scer\GAL4^eve.RN2 (Sanchez-Soriano et al., 2005) RP2 neuron & neurite, with Scer\GAL4^eve.RN2 (Sanchez-Soriano et al., 2005) somatic muscle, with Scer\GAL4^how-24B (Luo et al., 1994) tergal depressor of trochanter muscle motor neuron & dendrite, with Scer\GAL4^{shakB.lethal.4.1} (Jacobs et al., 2000) ventral nerve cord commissure \| embryonic stage 16, with Scer\GAL4^ftz.ng (Dorsten et al., 2007) vMP2 neuron, with Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) wing, with Scer\GAL4^Bx-MS1096 (Baron et al., 2000)
Detailed Description
	Statement Reference 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. (Jean et al., 2012) 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. (Nahm et al., 2010) 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. (Atwood et al., 2007) Stage 16 embryos overexpressing Cdc42[V12.Scer\UAS] driven by Scer\GAL4[ftz.ng] display axon bundles that cross the midline inappropriately. (Dorsten et al., 2007) 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. (Schafer et al., 2007) 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. (Taniguchi et al., 2007) Expression of Cdc42^V12.Scer\UAS in border cells, driven by Scer\GAL4^slbo.2.6 does not affect the formation of the egg chamber apical cap or the migration of the border cell cluster to the oocyte. (Medioni and Noselli, 2005) Dendrites of aCC and RP2 neurons expressing Cdc42^V12.Scer\UAS under the control of Scer\GAL4^eve.RN2 are irregular and shorter than wild-type dendrites. Scer\GAL4^eve.RN2 > Cdc42^V12.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. (Sanchez-Soriano et al., 2005) The antennal lobes of Cdc42^V12.Scer\UAS; Scer\GAL4^SG18.1 flies lack discernible glomeruli. Instead there are a clear glomerular-like structures within the antennal commissure where axons ectopically terminate. (Jhaveri et al., 2004) 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. (Paladi and Tepass, 2004) Cdc42^N17.Scer\UAS when driven by Scer\GAL4^{nos.UTR.T:Hsim\VP16} has no effect on transepithelial migration of germ cells in the embryo. (Kunwar et al., 2003) Cdc42^V12.Scer\UAS driven by Scer\GAL4^repo has no effect on the glia of the peripheral nervous system. (Sepp and Auld, 2003) When Cdc42^V12.Scer\UAS is driven by Scer\GAL4^ftz.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 Cdc42^V12.Scer\UAS is driven by Scer\GAL4^elav.PLu, no adults eclose. (Fritz and VanBerkum, 2002) Expression of Cdc42^V12.Scer\UAS driven by Scer\GAL4^332.3 does not affect either the dorsal cuticle or amnioserosa morphology. (Harden et al., 2002) 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. (Kim et al., 2002) 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]. (Wolf et al., 2002) 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. (Allen et al., 2000) When Cdc42^V12.Scer\UAS is driven by Scer\GAL4^Bx-MS1096, viable adults with a strong macrochaetae and microchaetae loss phenotype on the notum are produced. The wings on these animals are residual stumps. (Baron et al., 2000) Expression of Cdc42^V12.Scer\UAS under the control of Scer\GAL4^ey.PH results in an extreme reduction in the size of the eye disc. (Benlali et al., 2000) The tergotrochanteral muscle motorneuron cell bodies are present in flies expressing Cdc42^V12.Scer\UAS under the control of Scer\GAL4^{shakB.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. (Jacobs et al., 2000) When expression is driven by Scer\GAL4^dpp.blk1 aberrant and premature fusion of the mesothoracic ventral thoracic discs frequently occurs in L3 larvae. (Agnes et al., 1999) When driven in postmitotic neurons by Scer\GAL4⁶⁰, Cdc42^V12.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. (Gao et al., 1999) Most of the cuticles of embryos expressing Cdc42^V12.Scer\UAS under the control of Scer\GAL4^ptc-559.1 are distorted or missing. Embryos expressing Cdc42^V12.Scer\UAS under the control of Scer\GAL4^hs.PB (using heat shock) have a high frequency of puckers in the dorsal surface. (Harden et al., 1999) Expression of Cdc42^V12.Scer\UAS under the control of Scer\GAL4^48Y in the developing midgut does not result in accelerated migration of the endodermal midgut cells. (Martin-Bermudo et al., 1999) Scer\GAL4^elav.PLu-mediated expression causes arrest of late ISNb growth cone at contact with muscle 13. (Kaufmann et al., 1998) When driven by a Scer\GAL4 line expressed under the influence of an elav promoter, the SNb motor neuron bundle is missing. (Sone et al., 1997) Scer\GAL4⁴⁵⁸- or Scer\GAL4^hs.PB-mediated expression does not causes border cell migration defects. (Murphy and Montell, 1996) Spontaneous and evoked muscle contraction with Scer\GAL4^how-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\GAL4^how-24B a small number of larvae hatch that exhibit abnormal morphology of muscle fibres. (Luo et al., 1994)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has neuroanatomy defective \| embryonic stage 16 phenotype, suppressible \| partially by fra⁴/fra[+] (Dorsten et al., 2007)
NOT Enhancer of
Statement Reference Scer\GAL4⁶⁰/Cdc42^V12.Scer\UAS is a non-enhancer of neuroanatomy defective \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011)
Suppressor of
Statement Reference Scer\GAL4^He.PZ/Cdc42^V12.Scer\UAS is a suppressor of immune response defective \| recessive \| larval stage phenotype of Zir^BG00267 (Sampson et al., 2012)
Phenotype Manifest In
NOT Enhanced by
Statement Reference Cdc42^V12.Scer\UAS, Scer\GAL4^Gap1-NP3392 has anterior embryonic/larval midgut phenotype, non-enhanceable by puc^GS16811/puc[+] (Taniguchi et al., 2007)
Suppressed by
Statement Reference Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has dMP2 neuron phenotype, suppressible by chic^sand-1 (Fritz and VanBerkum, 2002) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has midline crossing tract \| embryonic stage 16 phenotype, suppressible \| partially by fra⁴/fra[+] (Dorsten et al., 2007) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has pCC neuron phenotype, suppressible by chic^sand-1 (Fritz and VanBerkum, 2002) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has ventral nerve cord commissure \| embryonic stage 16 phenotype, suppressible \| partially by fra⁴/fra[+] (Dorsten et al., 2007) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng has vMP2 neuron phenotype, suppressible by chic^sand-1 (Fritz and VanBerkum, 2002)
NOT suppressed by
Statement Reference Cdc42^V12.Scer\UAS, Scer\GAL4^Gap1-NP3392 has anterior embryonic/larval midgut phenotype, non-suppressible by puc^GS16811/puc[+] (Taniguchi et al., 2007)
Enhancer of
Statement Reference Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng is an enhancer of dMP2 neuron phenotype of Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng is an enhancer of pCC neuron phenotype of Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) Cdc42^V12.Scer\UAS, Scer\GAL4^ftz.ng is an enhancer of vMP2 neuron phenotype of Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is an enhancer of dMP2 neuron phenotype of Sos^e49 (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is an enhancer of pCC neuron phenotype of Sos^e49 (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is an enhancer of vMP2 neuron phenotype of Sos^e49 (Fritz and VanBerkum, 2002)
NOT Enhancer of
Statement Reference Scer\GAL4⁶⁰/Cdc42^V12.Scer\UAS is a non-enhancer of intersegmental nerve \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011) Scer\GAL4⁶⁰/Cdc42^V12.Scer\UAS is a non-enhancer of intersegmental nerve branch ISNb of A1-7 \| heat sensitive phenotype of N^l1N-ts1 (Song and Giniger, 2011) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-enhancer of dMP2 neuron phenotype of robo¹ (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-enhancer of pCC neuron phenotype of robo¹ (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-enhancer of vMP2 neuron phenotype of robo¹ (Fritz and VanBerkum, 2002)
Suppressor of
Statement Reference Scer\GAL4^btl.PS/Cdc42^V12.Scer\UAS is a suppressor \| partially of embryonic/larval dorsal trunk phenotype of bnl⁰⁰⁸⁵⁷ (Wolf et al., 2002) Scer\GAL4^hs.PB/Cdc42^V12.Scer\UAS is a suppressor of dorsal closure embryo phenotype of tkv⁷ (Ricos et al., 1999) Scer\GAL4^unspecified/Cdc42^V12.Scer\UAS is a suppressor of phenotype of ninaE¹⁷ (Chang and Ready, 2000)
NOT Suppressor of
Statement Reference Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-suppressor of dMP2 neuron phenotype of robo¹ (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-suppressor of pCC neuron phenotype of robo¹ (Fritz and VanBerkum, 2002) Scer\GAL4^ftz.ng/Cdc42^V12.Scer\UAS is a non-suppressor of vMP2 neuron phenotype of robo¹ (Fritz and VanBerkum, 2002) Scer\GAL4^twi.PG/Cdc42^V12.Scer\UAS is a non-suppressor of mesoderm phenotype of htl^AB42 (Wilson et al., 2005) Scer\GAL4^twi.PG/Cdc42^V12.Scer\UAS is a non-suppressor of mesoderm phenotype of stumps^09904b (Wilson et al., 2005)
Other
Statement Reference Cdc42^V12.Scer\UAS, Rac1^N17.hs, Scer\GAL4^hs.PB has embryonic/first instar larval cuticle \| dorsal phenotype (Harden et al., 1999) Cdc42^V12.Scer\UAS, Rac1^N17.hs, Scer\GAL4^hs.PB has embryonic/first instar larval cuticle phenotype (Harden et al., 1999)
Additional Comments
Genetic Interactions
Statement Reference 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. (Sampson et al., 2012) 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[60]). (Song and Giniger, 2011) Heterozygous fra[4] partially suppresses the incorrect midline crossing phenotype of ventral nerve cord axons in embryos overexpressing Cdc42[V12.Scer\UAS] via Scer\GAL4[ftz.ng]. (Dorsten et al., 2007) 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]. (Taniguchi et al., 2007) The addition of Cdc42^V12.Scer\UAS (driven by Scer\GAL4^ftz.ng) to robo¹/+ embryos has no effect on the midline crossover phenotype seen in the pCC/MP2 pathway axons. The addition of Cdc42^V12.Scer\UAS (driven by Scer\GAL4^ftz.ng) to Sos^e49 homozygous embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. All embryos exhibit the phenotype. The addition of chic^sand-1 to Cdc42^V12.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. (Fritz and VanBerkum, 2002) Expression of Cdc42[V12.Scer\UAS] under the control of Scer\GAL4[btl.PS] in a bnl[00857] background show occasional (4.4%) fusions of the adjacent lollipop-like dorsal trunk structures (bnl[00857] single mutants show no fusion of the adjacent metameric tracheal units). (Wolf et al., 2002) When Rac1^N17.hs is co-expressed with Cdc42^V12.Scer\UAS under the control of Scer\GAL4^hs.PB most cuticles are extremely disrupted. There is evidence of some rescue of the Rac1^N17.hs phenotype by Cdc42^V12.Scer\UAS expressed under the control of Scer\GAL4^hs.PB, as there are greater numbers of wild-type and mild dorsal closure defective embryos than seen with the expression of Rac1^N17.hs alone. (Harden et al., 1999) The dorsal closure phenotypes of tkv⁷ embryos are rescued by Cdc42^V12.Scer\UAS expressed under the control of Scer\GAL4^hs.PB. (Ricos et al., 1999)
Xenogenetic Interactions
Statement Reference The addition of Cdc42^V12.Scer\UAS to Ggal\MLCK^ct.Scer\UAS, Scer\GAL4^ftz.ng embryos enhances the midline crossover phenotype seen in the pCC/MP2 pathway axons. 97% of embryos exhibit the phenotype. An average of 7.8 crossovers are seen per embryo. (Fritz and VanBerkum, 2002)
Complementation & Rescue Data
Comments
Stocks ( 4 )
Bloomington	6287 w^*; P{UAS-Cdc42.V12}2 4854 w¹¹¹⁸; P{UAS-Cdc42.V12}LL1
Kyoto	108720 w^*; P{UAS-Cdc42.V12}2 107910 w¹¹¹⁸; P{UAS-Cdc42.V12}LL1
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	Cdc42^V12.Scer\UAS Cdc42^V12.UAS Cdc42^V12 (Kockel et al., 2001, Hutterer et al., 2004) Dcdc42 (Jhaveri et al., 2004) DCdc42^V12 (Medioni and Noselli, 2005)
Name Synonym
Secondary FlyBase IDs
	FBal0038152
References ( 49 )

Generate a list of	All references relating to this allele ( 49 )

List References by type	Research paper ( 48 ) Review ( 1 )
Recent research papers ( 4 )
	Fletcher et al., 2012, Curr. Biol. 22(12): 1116--1122 Positive feedback and mutual antagonism combine to polarize crumbs in the Drosophila follicle cell epithelium. [FBrf0218646] Jean et al., 2012, Mol. Biol. Cell 23(14): 2723--2740 Sbf/MTMR13 coordinates PI(3)P and Rab21 regulation in endocytic control of cellular remodeling. [FBrf0218866] Sampson et al., 2012, Dev. Comp. Immunol. 38(1): 160--168 The RhoGEF Zizimin-related acts in the Drosophila cellular immune response via the Rho GTPases Rac2 and Cdc42. [FBrf0219019] 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] Show all research papers ...
Recent reviews (0)
	All reviews listed in FlyBase were published before 2011 Show reviews ...

Allele Dmel\Cdc42V12.Scer\UAS

Allele Dmel\Cdc42^V12.Scer\UAS