The expression of DCTN1-p150Δ.Scer\UAS under the control of Scer\GAL4shot-OK307 results in shorter and thinner giant fiber terminals, as compared to controls. Expression under the control of Scer\GAL4GMR68A06 leads to a severe impairment of the axonal transport of Nrg-positive vesicles in giant fibers, as compared to controls.
Expression of GlΔ.Scer\UAS under the control of Scer\GAL4D42 results in a reduced number of type 1b boutons at the neuromuscular junction in third-instar larvae.
Third instar larvae expressing GlΔ.Scer\UAS under the control of Scer\GAL4D42 have axonal blockages.
Centrosome dynamics during cell division in pI (sensory organ precursor) cells in the notum expressing GlΔ.Scer\UAS under the control of Scer\GAL4neur-P72 proceed normally from prophase to anaphase. However, in telophase both centrosomes fail to move towards the apex of the pI daughter cells.
Survival data from virgin females expressing GlΔ.Scer\UAS under the control of Scer\GAL4RapGAP1-OK6 generated on standard laboratory food demonstrate that Gl1 mutants have significant reduction in survival including changes in median and maximum lifespan compared with wild-type.
Survival data from virgin females expressing GlΔ.Scer\UAS in motor neurons under the control of Scer\GAL4D42 generated on standard laboratory food demonstrate that Gl1 mutants have significant reduction in survival including changes in median and maximum lifespan compared with wild-type.
Flies expressing GlΔ.Scer\UAS in CM9 motor neurons under the control of Scer\GAL4E49 exhibit an accelerated decline in motor function with age. Quantification of the proboscis extension reflex shows no significant difference at 7 and 21 days of age between mutant and control flies. However, analysis from days 21 and 42 show an accelerated deterioration of proboscis extension in Scer\GAL4E49>GlΔ.Scer\UAS flies which results in a highly significant reduction in the rate of motor reflex response.
Flies expression Scer\GAL4E49>GlΔ.Scer\UAS exhibit progressive deterioration of proboscis muscle CM9 neuromuscular junctions (NMJs). Unlike in wild-type, synaptic area significantly decreases in the mutant with age. The mutant presynaptic nerve terminals appear disorganised in 72 day old flies compared with wild-type. The mutant NMJs display significantly more presynaptic sprouts per CM9 NMJ compared with controls at both 21 and 42 days of age. The number of synaptic retractions per CM9 NMJ is only increased at 42 day old mutant NMJs compared with wild-type. No abnormal age related changes are seen in the number of myo-nuclei, or gross organization of T-tubules in the mutant muscle compared to wild-type. Bristle-tracking reveals that Scer\GAL4E49>GlΔ.Scer\UAS flies have a significant reduction in average proboscis velocity compared with age-matched controls.
Scer\GAL4E49>GlΔ.Scer\UAS mutant CM9 NMJs have impaired neurotransmission. The average amplitudes of evoked endplate junctional potentials (EJPs) are significantly reduced at NMJs from Scer\GAL4E49>GlΔ.Scer\UAS flies compared with wild-type. The amplitudes of miniature EJPs (mEJPs), also referred to as quantal size, are found to significantly reduced at the NMJs in the mutant flies raised at diluted (0.5X) diet compared with wild-type flies on the same diet. Analysis of quantal content, a measure of presynaptic release determined by dividing the EJP amplitudes by the mEJP amplitudes, reveals no significant difference in vesicle release in mutant flies compared to controls.
Expression of GlΔ.Scer\UAS under the control of Scer\GAL4OK6 results in neuromuscular junctions indistinguishable from wild-type. At 7 and 9 hours after puparium formation there is no obvious change in synaptic vesicle distribution (compared to a redistribution in wild-type). These mutants also show considerably larger synaptic areas compared to wild-type.
Axonal sprouting of the injured axon after a crush injury to the segmental nerve in third instar larvae is significantly inhibited in animals expressing GlΔ.Scer\UAS under the control of Scer\GAL4unspecified.
Expression of GlΔ.Scer\UAS under the control of Scer\GAL4GMR.PF results in adult flies with smaller eyes than normal. The eyes contain fused ommatidia and misarrayed eye bristles.
Adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 have defects in giant fiber axon morphology; the characteristic terminal bend is missing and the axon tips are swollen.
Adults expressing GlΔ.Scer\UAS under the control of Scer\GAL4A307 have electrophysiological defects in the giant fiber system; some flies fail to respond to brain stimulation and those that do respond show a long response latency and show only a single response or poor following to repetitive stimuli
Targeted expression of GlΔ.Scer\UAS driven by Scer\GAL4αTub84B.PP results in abnormalities in the architecture of the CSD interneuron (CSDn). The ipsilateral dendrites are greatly increased in number and the presynaptic terminals are reduced compared to wild-type.
Expression of GlΔ.Scer\UAS in the developing eye using the MARCM system (under the control of Scer\GAL4Act5C.PP) has a modest effect on R7 tiling.
In the retinal photoreceptors of late third instar GlΔ.Scer\UAS; Scer\GAL4Glass38-1 larvae, the region of the photoreceptor containing the nucleus often leaves the retina and travels through the optic stalk towards the brain. Bolwig's organ photoreceptor nuclei in second instar GlΔ.Scer\UAS; Scer\GAL4elav.PLu larvae are mislocalised: instead of being located at the anterior tip of the larva they sit on the surface of the eye/antennal disc.
When GlΔ.Scer\UAS is driven by Scer\GAL4dimm-929 animals survive to pupal stage and about 50% eclose. Many of the eclosed adults exhibit uncoordinated movements and some do not inflate their wings.
GlΔ.Scer\UAS; Scer\GAL4elav-C155 animals have normal patterns of motor neuron fasciculation and innervation of target muscles. However at the third instar larval stage they have small synapses at neuromuscular junctions and detachments of the pre- and postsynaptic membrane around active zones.
The addition of GlΔ.Scer\UAS driven by Scer\GAL4elav-C155 leads to an increase in synaptic fingerprints (seen after synapses retract) at the synapses of muscles 6 and 7. No significant effect is seen on numbers of apoptotic nuclei in these animals. There are disruptions seen specifically in the presynaptic microtubule skeleton. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155, a reduction of more than 30% is seen in boutons per synapse (at the neuromuscular junctions of muscles 6 and 7). Active zone number per bouton is also decreased by about 50% compared to wild-type. Presynaptic boutons are filled with large vesicles and vacuoles of varying size. Post-synaptically the subsynaptic membrane folds (SSR) are much less compact than seen in wild-type, and can be invaded my mitochondrion. In the distal regions of the synapse, with severe SSR disruption, the presynaptic profiles are often very small and devoid of fully formed active zones. Also an 8 fold increase in the percentage of active zone that is detached is seen. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155, No alteration is seen in quantal size or mEPSP frequency, but quantal content is reduced by about 40%. When GlΔ.Scer\UAS is driven by Scer\GAL4elav-C155 no effect on synaptic development or bouton size is seen.
When expression is driven by Scer\GAL4c311 and the larvae raised at 29oC the larval lethality is fully penetrant and the eye disc phenotype is severely enhanced. Morphogenetic furrow progression is reduced or eliminated, and mitotic patterns are disrupted. Eye development is not completely blocked.
When expression is driven in the eye by Scer\GAL4GMR.PF or Scer\GAL4hs.2sev the eyes are reduced and roughened. When expression is driven by Scer\GAL4A307 the giant fibers fail to show their characteristic bend in the second thoracic neuromere, and the axons have swellings at their terminals of up to three times the normal axon diameter. The axons are distorted by large vesicles. Arborization of the dendritic field is normal. When expression is driven by Scer\GAL4c17 a similar, though less extreme, phenotype is seen to that caused when expression is driven by Scer\GAL4A307. These abnormalities in giant fibers appear late in development. Morphology is normal up to 24hr APF, indicating no defects in growth and pathfinding in the brain and connective. By 48hr APF the defects are becoming apparent. When expression is driven by Scer\GAL4c17 or Scer\GAL4A307 dye coupling between the giant fibre and the TTM (tergotrochanteral motoneuron) is reduced and abolished, respectively. When expression is driven by Scer\GAL4c17 or Scer\GAL4A307 and the GF-TTM synapse characteristics are examined, changes occur in response latency (becomes variable), refractory period (increased) and following frequency (decreased). The effect is more pronounced for Scer\GAL4A307 than for Scer\GAL4c17. DLM muscle response is normal.