Scer\GAL4ppk.PG-mediated overexpression of Rac1Scer\UAS.cLa drives ectopic dendrite branching, although total dendrite length is unaffected. This increase in terminal dendrite branching is accompanied by a significant decrease in primary dendrite growth - as a result, distal portions of the territory normally covered by C4da neurons are completely devoid of dendrites.
Overexpressing Rac1Scer\UAS.cLa in class IV da neurons (Scer\GAL4ppk.PU) partially (increased regeneration percentage but not terminal branching or commissure growth) improves axon regeneration.
Overexpression of Rac1Scer\UAS.cLa driven by Scer\GAL4109(2)80 leads to a significant increase in dendrite branch points (but not length) in class I da sensory neurons compared to wild type.
Class III ddaA neurons expressing Rac1Scer\UAS.cLa under the control of Scer\GAL41003.3 show a dramatic increase in the number of dendritic sensory filopodia compared to wild type. These filopodia are dynamic and their stability is not altered compared to controls. The average length of the filopodia is significantly decreased compared to wild type, while the total length of primary dendritic branches is not altered.
Larvae expressing Rac1Scer\UAS.cLa under the control of Scer\GAL41003.3 are hypersensitive to gentle touch compared to controls.
Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4ppk.PG promotes F-actin structure formation in the distal dendrites of dorsal cluster neurons.
Overexpression of Rac1Scer\UAS.cLa in many neuron types, including the da neurons, under the control of Scer\GAL4477, leads to hyperbranching of dendrites.
Expression of Rac1Scer\UAS.cLa under the control of the neuronal drivers Scer\GAL4BG380, Scer\GAL4OK6 or Scer\GAL4elav-C155 leads to neuromuscular junction overgrowth during larval development, resulting in an increase in the number of synaptic boutons, branches and the appearance of abnormal synaptic protrusions. No overgrowth is seen when Rac1Scer\UAS.cLa is expressed in muscle under the control of the Scer\GAL4Mhc.PW driver.
Expression of Rac1Scer\UAS.cLa under the control of either Scer\GAL4BG380 or Scer\GAL4OK6 produces increased mean evoked excitatory junctional potentials (EJPs) and quantal content in third instar larvae compared to controls. The size of miniature excitatory junctional potentials (mEJPs) does not differ from controls.
Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4DB331 does not alter the overall dendritic architecture in the lobular plate tangential cells; neither the position not branching patterns of primary and secondary order dendrites are affected. However, there is an increase in spine density and a change in spine morphology (the spines appear shorter and less well defined) compared to controls.
Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4221 in class I neurons promotes de novo branch initiation reminiscent of, but not identical to, the filopodia of class III neurons.
Expression of Rac1Scer\UAS.cLa under the control of cer\GAL4ato.3.6 inhibits the extension of axons from dorsal cluster neurons (DCNs), with an average of only 7.8 axons crossing toward the medulla instead of the wild-type average of 11.7. Expression of this transgene also results in a decreased number of DCN axons crossing the optic chiasm at 20%-30% pupal development.
Expression of Rac1Scer\UAS.cLa, under the regulation of Scer\GAL4109(2)80, dramatic increases in larval neurons dendritic branching are observed. This is due to the formation of filopodia on normally non-filopodia bearing neurons (non-class III dendritic arborisation neurons), without altering the filopodia density. This branching phenotype becomes apparent in newly-hatched first instar larvae. Rac1Scer\UAS.cLa expression, under the regulation of Scer\GAL4109(2)80, like CaMKIIT287D.Scer\UAS expression, increases actin turnover, although the effects on morphological stability are significantly different.
Expression of Rac1Scer\UAS.cLa under the control of Scer\GAL4GMR.PF results in about 90% pupal lethality. Escaper adults have strongly reduced eyes with no organised structure.
When expression is driven by Scer\GAL4He.PZ, hemocyte proliferation and lamellocyte numbers are increased, and crystal cells are unaffected. Melanotic masses form. Similar, though milder, effects are seen when expression is driven by Scer\GAL4Hml.PG.
Targeted expression of Rac1Scer\UAS.cLa to the GF under the control of Scer\GAL4A307 results in over 95% of GF axons showing morphological aberrations whereas less than 15% of controls show defects. In the majority of specimens the axons grow out of the brain and into the second thoracic neuromere (T2) but fail to make the terminal bend that is characteristic of the gf presynatpic terminal. In addition the tips of the axons appear swollen and contain vesicle-like structures. Nine percent of axons fail to exit the brain and often cross the midline and project into the contralateral half of the brain.
Over 90% of GFs in Scer\GAL4A307; Rac1Scer\UAS.cLa adult brains exhibit abnormalities. Although neurite outgrowth and branching appears normal, and the three major dendritic domains are always discernible, typically dendrite are thickened and display inappropriate minor branches. Swollen dendrites containing large vesicle-like structures are also observed.
When Scer\GAL4A307; Rac1Scer\UAS.cLa flies are tested physiologically, they all exhibit a TTM response latency that is more than twice that of control flies. The fidelity of transmission for repetitive stimuli is also reduced and in most cases only a single response to the first stimulus occurs.
Approximately 30% of Scer\GAL4c17; Rac1Scer\UAS.cLa GF axons exhibit a bendless phenotype with swollen terminals and no lateral bends while the remaining axons appear wild-type.
Approximately 81% of Scer\GAL4A307; Rac1Scer\UAS.cLa flies exhibit a bendless GF phenotype, while 64% of Scer\GAL4A307; Rac1Scer\UAS.cLa GFs are bendless. The remainder exhibit wild-type bends or large abnormally shaped processes in the target region.
Expression is driven by Scer\GAL4en-e16E causes wing vein thickening, extra sensory organs and wing enlargement.