The adulthood-only expression of Rac1V12.Scer\UAS under the combined control of Scer\GAL4ey-OK107 and Gal80[ts] leads to a severe decrease in intermediate-term olfactory memory (3h after conditioning), as compared to controls.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4GMR13F02 (in combination with a Gal80[ts] transgene to restrict expression to the adult stage) results in decreased memory after conditioning in an olfactory conditioning assay.
Expression of Rac1V12.Scer\UAS driven by Scer\GAL4hs.2sev causes defects in ommatidial rotation (planar cell polarity-like defects) and R-cell loss in the adult eye.
Adult mushroom body specific (using Scer\GAL4Mef2.247.Switch adults fed mifepristone/RU486) Rac1V12.Scer\UAS knockdown causes loss of acquired ethanol preference, as is seen in wild type (show increased ethanol consumption over 4 days); mutant flies have normal naive ethanol preference.
The mushroom body axons of flies expressing Rac1V12.Scer\UAS under the control of Scer\GAL4ey-OK107 fail to extend to form peduncles and lobe structures (the 'posterior arrest' phenotype). Scer\GAL4ey-OK107>Rac1V12.Scer\UAS expressing clones that exhibit the posterior arrest phenotype display ectopic regions of F-actin in the posteriorly arrested axons.
Primary macrophages isolated from animals expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Cg.PA have an excess number of F-actin rich protrusions compared to wild type.
Expression of Rac1V12.Scer\UAS in the haemocytes under the control of Scer\GAL4crq.PO results in a failure of haemocyte migration into the posterior half of the embryo. These embryos also display a failure of anterior Malpighian tubule migration into the anterior half of the embryo. In these animals, the anterior pair of tubules projects into the posterior half of the embryo.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 blocks the transepithelial migration of germ cells leading the majority of germ cells to adhere to each other inside the midgut at late stages. The few germ cells that do manage to cross the gut epithelium are scattered in the soma at stage 16.
Conditional expression of Rac1V12.Scer\UAS under the control of Scer\GAL4ey-OK107 (using tub-Gal80[ts] to limit the expression to the adult stage) results in accelerated memory decay compared to controls although the immediate memory (3 and 15 in after training) is not affected. The sensimotor responses or mushroom body morphology are also not impaired. The Rac1V12.Scer\UAS expressing flies perform better compared to controls in an reversal learning aversive olfactory assay (in which the odor-shock contingency is reversed in each training session).
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4Gap1-NP3392 results in defects in the left-right asymmetry of the anterior midgut. 13% of embryos show inversion of the normal left-right asymmetry and 5% show no left-right asymmetry.
Expression of Rac1V12.Scer\UAS, under the control of Scer\GAL4ato.3.6, induces premature and severe retraction of dorsal cluster neuron axons visible even at L3.
When Rac1V12.Scer\UAS is expressed in the caudal visceral mesoderm (CVM) cells under the control of Scer\GAL4447.2 they fail to migrate towards the anterior pole of the embryo. The CVM cells remain viable at the posterior end of the embryo, indicating that cell survival is unaffected.
Expression of vavΔ1-207.Scer\UAS.T:Ivir\HA1 under the control of the tracheal system driver Scer\GAL4btl.PS results in a variety of defects in the embryo including truncation of the tracheal dorsal trunk in some segments and severely misguided dorsal branching.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4wg.PM does not block cuticle secretion in embryos, but instead causes excess specification of denticles.
Expression of Rac1V12.Scer\UAS in border cells, driven by Scer\GAL4slbo.2.6, causes a border cell cluster migration defect in over 50-60% of egg chambers. However, the apical cap of these egg chambers forms and is shed normally.
Expression of Rac1V12.Scer\UAS, under the control of the hemocyte-specific driver Scer\GAL4crq.PO, inhibits hemocyte migration in the embryo by stage 14. Hemocytes begin migration out of the head region, but then lose polarized migration and accumulate in the anterior of the embryo. At stage 17, the ventral nerve cord is shorter in Rac1V12.Scer\UAS embryos than in wild-type, indicating that the VNC fails to condense correctly in Rac1V12.Scer\UAS mutants. Expression of Rac1V12.Scer\UAS in the lateral glia, driven by Scer\GAL4158, results in inhibition of VNC condensation in embryos but does not affect the pattern of axon tracts within the VNC. The differentiation and survival of the lateral glial cells are also unaffected. Expression of Rac1V12.Scer\UAS throughout the CNS, driven by Scer\GAL4elav-C155, inhibits VNC condensation and disrupts the pattern of axon tracts within the VNC.
Expression of Rac1V12.Scer\UAS in segmental stripes of the embryonic epithelium, driven by Scer\GAL4en-e16E, allows the embryo to survive to the dorsal closure stage. The leading edge cells of these embryos show produce larger lamellipodia than wild-type cells and appear to have a migrational advantage over neighbouring wild-type cells, so that the Scer\GAL4en-e16E stripes fuse with one another, resulting in almost all of the leading edge expressing Rac1V12.Scer\UAS. This leads to premature termination of dorsal closure, leaving a large hole in the dorsal epithelium.
When Rac1V12.Scer\UAS is driven by Scer\GAL4hs.PB (and heat shock) excessive contraction of the amnioserosa is seen. Also loss of cuticle secretion is seen.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4gcm-rA87.P blocks macrophage migration in embryos; most macrophages are unable to migrate and remain clustered anteriorly.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4Cg25C-A109.1F2.P causes strong clustering of macrophages in the embryo, resulting in large regions of the embryo that are devoid of macrophages at stage 17. The macrophages extend longer, more prominent cellular protrusions than in wild type, and have a more elongated, spindle-like shape than in control embryos.
Macrophages expressing Rac1V12.Scer\UAS under the control of Scer\GAL4unspecified show strongly elevated levels of cortical F-actin compared to wild type. The macrophages that cluster around the foregut in these mutant embryos form an excessive number of lamellipodia. Some of the mutant macrophages contain two nuclei.
Rac1V12.Scer\UAS expression causes Tv axons to stall before reaching the midline and fail to innervate the dorsal neurohemal organs.
After late stage 12 the tracheal primordia of Rac1V12.Scer\UAS; Scer\GAL4btl.PS embryos lose their branched morphology: cells budding from the tracheal primordia remain attached by thin stalks of cytoplasm for around 30 minutes before being expelled into the body cavity. This process is co-incident with a loss of polarity in these cells. By stage 15 the tracheal primordia fuse together to form one or two cell clusters on either side of the body cavity.
When Rac1V12.Scer\UAS is driven in the eye by Scer\GAL4GMR.PF, a mild rough eye phenotype and a complete loss of ommatidia is seen in the posterior region. When Rac1V12.Scer\UAS is driven by Scer\GAL4elav-C155, 29% of ISNb are arrested at the site of contact with ventral longitudinal muscle 13 before reaching their final target, muscle 12. No midline crossing longitudinal connectives is seen.
When Rac1V12.Scer\UAS is driven by Scer\GAL4repo in embryos, they display collapsed glial sheaths as well as PNS glial migration defects. The lateral line glia fail to connect across hemi-segments.
Expression of Rac1V12.Scer\UAS, driven by Scer\GAL4332.3 results in failure to secrete cuticle in 41% of embryos. In embryos which do manage to secrete cuticle, 47% show puckering of the dorsal surface. In early stage 14 embryos Rac1V12.Scer\UAS expression, driven by Scer\GAL4332.3, results in contraction of the amnioserosa, with greatly constricted cells that occupy less than half of the dorsal hole at its posterior end. In wild-type embryos, only the end amnioserosa cells constrict but Rac1V12.Scer\UAS overexpression causes constriction of all cells. A similar effect is seen when Rac1V12.Scer\UAS expression is induced through heat shock by the Scer\GAL4hs.PB driver. In stage 15 embryos expressing Rac1V12.Scer\UAS driven by Scer\GAL4332.3 there is bunched closure of the epidermis around the amnioserosa causing the embryos to become bowed, with their heads and tails pulled in towards each other. This effect is likewise seen in embryos where Rac1V12.Scer\UAS expression is driven by Scer\GAL4hs.PB. Although overexpression of Rac1V12.Scer\UAS driven by Scer\GAL4c381 does not cause failure of cuticle formation, cuticles show puckers extending out from the dorsal surface. Such embryos fail to undergo germband retraction but are able to complete dorsal closure. As with expression driven by Scer\GAL4332.3, Scer\GAL4c381-driven expression of Rac1V12.Scer\UAS causes the same bunched closure of the epidermis and contraction of the amnioserosa.
Expression of Rac1V12.Scer\UAS under the control of Scer\GAL4SG18.1 has no effect on the peripheral organisation of the olfactory neurons, but the neurons are disturbed within the olfactory lobe and the inter-antennal commissure is not formed.
Clones of cells expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Act5C.PP are not recovered in the nurse cell follicle cells. Clones of cells expressing Rac1V12.Scer\UAS under the control of Scer\GAL4Act5C.PP in the posterior follicle cells but not in the main body portion result in posterior cells both in and adjacent to the clone delaminating and leaving the continuous follicle epithelium.
Scer\GAL4A307; Rac1V12.Scer\UAS flies at 25[o]C do not survive till adulthood. Adult progeny raised at 18[o]C exhibit gross GF abnormalities, with no neurite extensions.
Frequent defects in the projection pattern of VUM neurons are seen in stage 14 embryos expressing Rac1V12.Scer\UAS under the control of Scer\GAL4sim.PS. At stage 16, a fused commissure phenotype is seen.
Expression of Rac1V12.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-C155-mediated expression causes arrest of the ISNb growth cone when it contacts with muscle 14.
Scer\GAL4how-24B-mediated expression causes myoblasts to distribute into groups at locations corresponding to ventral, lateral and dorsal muscle groups and the myoblasts generally fail to fuse. 10% myoblasts do fuse forming rudimentary myotubes, the remaining unfused cells have a more elongated morphology. Many prefusion complexes are present, electron dense membrane plaques are present and cells appear to elongate and align normally. However, only in a few cases does the plasma membrane vesiculate in any serious way, few membrane pores are observed. By stage 14 many myoblasts are dead, dying or cleared by macrophages.
When driven by a Scer\GAL4 line expressed under the influence of an elav promoter, the SNb motor neuron bundle is missing.
Scer\GAL4198Y-mediated expression does not causes border cell migration defects.
Embryos exhibit spontaneous and evoked muscle contraction with Scer\GAL4elav.PLu and Scer\GAL460, little muscle contraction with Scer\GAL41407 and no muscle contraction, abnormal gut and tracheae with Scer\GAL4how-24B (the segmentally repeated myoblast cells fail to fuse with each other). When in combination with Scer\GAL41407 one copy of Rac1L89.Scer\UAS causes some axonal loss between the lateral and dorsal clusters, two copies causes greater loss. One copy of Rac1Scer\UAS.cLa ameliorates this axonal loss. Scer\GAL4elav.PLu causes permanent arrest of the axons moving from the dorsal to lateral cluster.