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