Haemocytes bled from homozygous third instar larvae expressing Rho1V14.Scer\UAS under the control of Scer\GAL4srp.Hemo show a marked increase in the number of filopodia compared to control haemocytes.
Scer\GAL4btl.PS-mediated expression of Rho1V14.Scer\UAS causes fusion defects in the tracheal dorsal trunk and lateral trunk and extension defects in the ganglionic branch.
Flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a do not show significant neural vacuolization after 5 days as adults.
Flies expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Appl.G1a do not perform well in a fast phototaxis assay but do not reveal significant neural vacuolization.
Pan-neuronal expression of constitutively active Rho1V14.Scer\UAS (under the control of Scer\GAL4Appl.G1a) does not result in vacuoles in young (5 day old) flies. A few vacuoles are detectable in 14 day old flies, in contrast to age-matched controls. The total size and number of vacuoles are significantly increases in Rho1V14.Scer\UAS-expressing flies compared to controls.
Expression of the constitutively active Rho1V14.Scer\UAS transgene in the developing eye under the control of Scer\GAL4GMR.PF results in dramatic nervous system degeneration in young flies. This affects the development of the retina, causing a smaller and severely rough eye. The retina is also much thicker in these mutants.
Expression of Rho1V14.Scer\UAS in motor neurons under the control of Scer\GAL4BG380 does not result in any neuromuscular junction overgrowth during larval development.
Animals carrying Rho1V14.Scer\UAS, Scer\GAL4ptc-559.1 and Scer\GAL80ts.αTub84B which have been shifted to 29[o]C to inactivate Scer\GAL80ts.αTub84B and allow expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ptc-559.1 for 2-8 hours during the pupal stage show wings with cells that bulge apically, forming multiple wing hairs (the cells can have 10 or more short hairs) of relatively normal polarity. Most of the cells form hairs on the distal side, but some show hair formation at an alternative face/vertex, most often 60[o] from distal. The cells have increased cortical F-actin staining and decreased cytoplasmic actin staining. In some cases, cells appear to be expelled from the epithelium.
Clones in the wing expressing Rho1V14.Scer\UAS under the control of Scer\GAL4Act have an extreme multiple hair phenotype and a bulged cell surface.
Expression of Rho1V14.Scer\UAS in the border cells under the control of Scer\GAL4slbo.2.6 results in clusters with tightly rounded border cells and no large actin protrusions are observed. 50% of clusters show delays in migration.
Stage 16 embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4ftz.ng display very few ventral nerve cord axon bundles that inappropriately cross the midline.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Gap1-NP3392 results in defects in the left-right asymmetry of the anterior midgut. 6% of embryos show inversion of the normal left-right asymmetry and 1% show no left-right asymmetry.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4ems.HRE blocks basolateral elongation and impairs cell invagination in the posterior spiracle. Very disorganised and superficially localised Filzkorper are formed in these embryos.
Mutant germ cells successfully transmigrate the posterior midgut during stages 9 and 10 of embryogenesis, but subsequently some germ cells fail to move from the posterior midgut into the mesoderm.
When Rho1V14.Scer\UAS is driven by Scer\GAL4repo the peripheral glia do not migrate peripherally as normal, manifesting as dense clusters of glia arrested at their birth place at the CNS/PNS transition zone. Typically long actin containing fibres extend out of the glial clusters, and there are large expanses of PNS tracts with no glial sheaths whatsoever. The aberrant spike structures of the peripheral glia do not always project along sensory axon pathways. The lateral line glia fail to extend processes to interconnect between hemisegments and lateral chordotonal PNS glial cells appear collapsed and rounded, although their associated lateral chordotonal neurons appear properly formed. The sensory axon tracts in these mutants appear defasciculated although their pathfinding to the CNS is generally normal. The glial stalling phenotype is highly penetrant (97%).
Expression of Rho1V14.Scer\UAS, under the control of Scer\GAL4repo, in embryonic glia prevents extension of cytoplasmic processes and causes glial cell bodies to be stalled in the CNS-PNS transition zone. The distance between glia and sensory neuron birthplaces is much greater than the length of growth cones or their filopodial reach. Sensory axon pathways to the CNS are organized as in wild type, except that the axon tracts are defasciculated.
Leading edge cells expressing Rho1V14.Scer\UAS under the control of Scer\GAL4en-e16E are more constricted than their wild-type neighbors at early stages of dorsal closure. They subsequently take on irregular shapes and are outcompeted during dorsal closure, such that wild-type stripes tend to dominate the leading edge. Thus, when dorsal closure is complete, the midline seam epithelium is largely wild-type.
Lumen formation is blocked at all anastomosis sites in the tracheal system in embryos expressing Rho1V14.Scer\UAS under the control of Scer\GAL4btl.PS. Tracheal branch migration is modestly attenuated but the pattern of primary and secondary branching is not detectably affected in these embryos.
A few adult escapers are seen at 18oC when Rho1V14.Scer\UAS is expressed under the control of Scer\GAL4OK107. These flies have complex mushroom body defects.
Expression of Rho1V14.Scer\UAS under the control of Scer\GAL4Tab2-201Y results in a 50% reduction in the volume of the dendritic field in the mushroom body neurons expressing Rho1V14.Scer\UAS. No abnormality in axonal projections is seen. There is no change in the total number of mushroom body neurons. When Rho1V14.Scer\UAS is expressed under the control of Scer\GAL4Tab2-201Y in a single mushroom body clone, the dendritic volume appears unaffected, but there is a 50% reduction of dendritic density. There is no change in the total number of mushroom body neurons.