Allele Dmel\Cdc42^F89.Scer\UAS

General Information
Symbol	Dmel\Cdc42^F89.Scer\UAS	Species	D. melanogaster
Name		FlyBase ID	FBal0062059
Feature type	allele	Created / Updated	2006-08-20/2006-08-20
Associated gene	Dmel\Cdc42

Allele class
Mutagen	in vitro construct \| regulatory fusion
Nature of the Allele
Allele class
Mutagen	in vitro construct \| regulatory fusion (Eaton et al., 1995, Eaton et al., 1996)
Mapped Features and Mutations
Type Symbol & 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 Amino acid replacement: S89F. (Luo, 2001.5.2) Construct: A dominant negative form of Cdc42 is expressed under the control of Scer\UAS regulatory sequences. (Eaton et al., 1995) A dominant negative form of Cdc42 is expressed under the control of Scer\UAS regulatory sequences. (Eaton et al., 1996)
Assay mode	In transgenic Drosophila (intraspecific) (Eaton et al., 1996, Eaton et al., 1995)
Carried in construct	P{UAS-Cdc42.F89} (Medioni and Noselli, 2005, Jacinto et al., 2000, Luo, 2001.5.2, Eaton et al., 1995, Eaton et al., 1996, Stramer et al., 2005, Hozumi et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	cell polarity defective, with Scer\GAL4^Pxn.PS, Scer\GAL4^crq.PA (Stramer et al., 2005)
Phenotype Manifest In
	microchaeta & wing, with Scer\GAL4^ptc-559.1 (Eaton et al., 1996, Eaton et al., 1995) dorsal mesothoracic disc \| anterior/posterior compartment boundary, with Scer\GAL4^ptc-559.1 (Eaton et al., 1995) wing, with Scer\GAL4^ptc-559.1 (Eaton et al., 1995) embryonic epidermis \| dorsal, with Scer\GAL4^en-e16E (Jacinto et al., 2000) dorsal closure embryo, with Scer\GAL4^en-e16E (Jacinto et al., 2000) embryonic hemocyte & leading edge, with Scer\GAL4^Pxn.PS, Scer\GAL4^crq.PA (Stramer et al., 2005) embryonic hemocyte, with Scer\GAL4^Pxn.PS, Scer\GAL4^crq.PA (Stramer et al., 2005)
Detailed Description
	Statement Reference Causes an ectopic furrow to form at the anterior/posterior compartment boundary of the wing disc, when expressed using Scer\GAL4^ptc-559.1. Cells in the furrow (which are expressing Cdc42^F89.Scer\UAS) are shorter than normal and are bloated basally. 30% of wings derived from discs in which Cdc42^F89.Scer\UAS is expressed using Scer\GAL4^ptc-559.1 have blisters at the compartment boundary, caused by the dorsal and ventral surfaces of the wing separating. Hairs at the compartment boundary are often missing, the penetrance of this phenotype being highest proximally. (Eaton et al., 1995) Cells in the wing in which Cdc42^F89.Scer\UAS is expressed under the control of Scer\GAL4^ptc-559.1 either fail to form wing hairs or form short, deformed wing hairs which have a malformed base. These cells show abnormalities in actin distribution as hair development occurs. (Eaton et al., 1996) When Cdc42^F89.Scer\UAS is driven by Scer\GAL4^en-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. Also the fused seam normally seen where the two zipper-fronts meet is not seen. When the opposite segmental stripes are seen to fuse, some misalignment is seen. (Jacinto et al., 2000) Expression of Cdc42^F89.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) Hemocytes in embryos expressing Cdc42[F89.Scer\UAS] under the simultaneous control of both Scer\GAL4[Pxn.PS] and Scer\GAL4[crq.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 Cdc42[F89.Scer\UAS] under the simultaneous control of both Scer\GAL4[Pxn.PS] and Scer\GAL4[crq.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. (Stramer et al., 2005)
Interactions
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Comments
Stocks ( 1 )
Bloomington	6286 w^*; P{UAS-Cdc42.F89}3
Notes on Origin
Discoverer

Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym	Cdc42^F89.Scer\UAS Cdc42^S89.Scer\UAS Cdc42^S89.UAS Cdc42^S89 (Stramer et al., 2005) DCdc42^F.89 (Medioni and Noselli, 2005)
Name Synonym
Secondary FlyBase IDs

References ( 7 )
Research paper	Hozumi et al., 2006, Nature 440(7085): 798--802 An unconventional myosin in Drosophila reverses the default handedness in visceral organs. [FBrf0191242] Medioni and Noselli, 2005, Development 132(13): 3069--3077 Dynamics of the basement membrane in invasive epithelial clusters in Drosophila. [FBrf0187473] Stramer et al., 2005, J. Cell Biol. 168(4): 567--573 Live imaging of wound inflammation in Drosophila embryos reveals key roles for small GTPases during in vivo cell migration. [FBrf0184064] Jacinto et al., 2000, Curr. Biol. 10(22): 1420--1426 Dynamic actin-based epithelial adhesion and cell matching during Drosophila dorsal closure. [FBrf0131320] Eaton et al., 1996, J. Cell Biol. 135(5): 1277--1289 Roles for Rac1 and Cdc42 in planar polarization and hair outgrowth in the wing of Drosophila. [FBrf0090541] Eaton et al., 1995, J. Cell Biol. 131(1): 151--164 CDC42 and Rac1 control different actin-dependent processes in the Drosophila wing disc epithelium. [FBrf0083883]
Personal communication to FlyBase	Luo, 2001.5.2, Luo constructs and insertions. Luo constructs and insertions. [FBrf0136038]

Allele Dmel\Cdc42F89.Scer\UAS

Allele Dmel\Cdc42^F89.Scer\UAS