rut1 homozygous mutant adults have a similar increase in aversive olfactory 24 h memory observed when the recall environment better matches the training environment (presence of copper grid) to controls.
rut1 homozygous adults show significant decrease in the amnestic cooling sensitive memory component at 3 hr post-training in an olfactory memory assay compared to controls.
rut1 causes a mild neuromuscular junction (NMJ) undergrowth phenotype. Heterozygous rut1 larvae have NMJs that do not differ from wild-type.
rut1/rut1 mutant flies exhibit defective short term memory (3 min after odor training), defective midterm memory, and defective anaethesia-sensitive memory, but not defective anaesthesia-resistant memory, when cold-amnestic treatment is applied 30 min before testing 3 h odor memory, as compared to controls.
Compared with wild-type, rut1 mutants show a decrease in synaptic varicosity number when normalised to muscle surface area. In addition , they display a decrease in axonal branch number and innervation length.
rut1 mutants do not display any changes in synaptic morphology compared to wild-type.
rut1 mutants exhibit approximately 50% of the normal memory performance of wild-type controls, both immediately after a training session and 24 hours after spaced training. Extinction learning appears to be normal in these mutants. With either 10 or 30 sessions of extinction there is a significant inhibitory extinction in these mutants.
Mutants show a significant impairment in 3 minute memory after olfactory conditioning compared to wild-type flies.
Homozygous and rut1/rut2080 adults show severely reduced 2 minute memory after a single aversive Pavlovian training session. These adults also show severely reduced memory performance 24 hours after either ten massed or ten spaced sessions of training.
Aversive memory fails to form after associative linalool/quinine hemisulfate conditioning in rut1 mutant larvae.
rut1 flies show significantly lower learning after aversive olfactory conditioning (flies trained to associate odors with an electric shock) or after appetitive olfactory conditioning (with 1.0M sucrose presented with a conditioned odor), compared to controls.
rut1 mutant flies show decreased avoidance of low temperatures.
rut1 mutants exhibit significantly shorter life spans compared to controls.
rut1 flies exhibit a delay in recovery time from a 20 minute 37[o]C heat stress, as shown by a locomotive index generated with a climbing assay.
Mitochondrial aconitase activities in 30-day old rut1 flies are reduced by 75% compared to controls.
Superoxide levels are increased in rut1 flies compared to controls.
Homozygous rut1 mutants exhibit normal spontaneous odor identity discrimination.
Homozygous rut1 mutants exhibit disrupted conditioned odor identity discrimination.
rut1 mutant larvae, trained with LIN/SUC, LIN with DW, or SUC alone fail to exhibit a Response Index (RI) increase, unlike wild-type flies. The gustatory response for SUC is slightly lower in rut1 larvae than in wild-type flies.
Mutant larvae show no significant defects in synapse formation.
When raised at room temperature or at 25oC, the motor axon terminals of rut1 larvae show a similar level of arborization to wild-type larvae. However, the motor nerve termini of wild-type larvae raised at 30oC show greatly increased levels of branching and variscosities, while no such large increase in terminal projection.
Facilitation during tetanus is slightly reduced and post-tetanic potentiation is lacking in rut1 embryos. The frequency and amplitude of miniature synaptic currents (mSCs) is not significantly different from controls. However, in saline with high K+ the frequency of mSCs is lower than in controls.
Injection of serotonin or norepinephrine increases the heart rate in rut1 mutant pupae, and the change in rate is no different from that seen in wild-type controls.
Mutant flies show a significant increase in the number of rest hours per 24 hours compared to controls.
The electroantennogram (EAG) of mutant flies shows a slowed voltage change in response to ethyl acetate, with the correspondent rise time (RT) value becoming significantly different from wild type at the highest concentration of ethyl acetate used. At high concentrations of odorant, mutant flies are less sensitive to ethyl acetate than control flies in a behavioural assay. Sensitivity to acetone is reduced. Sensitivity to benzaldehyde is increased.
During 30 Hz stimulation of the neuromuscular junction, mobilisation and translocation of vesicles from the reserve pool (RP) to the exo/endo cycling pool (ECP) is depressed in rut1, resulting in a larger RP. Bafilomycin treated preparations from rut1 mutants stimulated at 1Hz for a prolonged period of time led to markedly decreased amplitude of evoked potentials, as seen in wild-type. Subsequent stimulation at 10Hz for 10s does not increase the amplitude in rut1, as compares to wild-type. However,, asn increase in the amplitude of evoked potentials is observed during and after the second or third application of 10Hz stimulation. Furthermore, when rut1 mutants which were pre-treated with bafilomycin and stimulated at 1Hz, is incubated with 300μM db-cAMP for 25 minutes, the amplitude of potentials evoked at 1Hz is not affected or slightly increased. However, the amplitude of potentials evoked at 10Hz for 10s gradually increases during stimulation, and the increase continues for about 30 s, as observed in wild-type.
The number of synapses per unit length of terminal is reduced greater than twofold compared to controls in both axons 1 and 2 (from neurons RP3 and 6/7b respectively) at the neuromuscular junction of muscles 6 and 7 of third instar rut1/Y larvae. Synapses of axon 1 are approximately threefold larger than controls and axon 2 terminals also show an increase in synapse size. The number of active-zone dense bars is increased compared to controls. A much greater variability in synapse area is seen compared to controls. The ratio of docked to undocked vesicles is lower than in wild type in axon 1 synapses. The frequency of spontaneous release (miniature excitatory junctional currents - mejcs) at the neuromuscular junction is reduced compared to wild type. There is a Ca2+-independent increase in the decay time of mejcs. Evoked ejcs show a high frequency of failures and reduced release. There is a significant reduction in the mean quantal content. The peak amplitude of evoked ejcs is consistently lower than in wild type. Broadened or multiple peaks occur in evoked ejcs. There is increased variability in the time to peak of evoked ejcs. There is a Ca2+-dependent increase in the decay time of evoked ejcs. Boutons show altered short-term plasticity.
The mean synaptic area for synapses in individual type Ib and Is varicosities is significantly increased in rut1 animals compared to controls. The number of dense bodies per synapse is modestly increased in type Ib but not in type Is varicosities.
The peak dihydropyridine (DHP)-sensitive current in rut1 larval muscles cannot be increased by application of 1μm forskolin.
rut1 larvae have fewer type Ib and type Is varicosities at the neuromuscular junction of muscles 6 and 7 of abdominal segment 4 compared to wild type. There is a reduction in excitatory junction potential (EJP) amplitude at muscles 6 and 7 compared to wild type.
rut1 flies have calyxes that are reduced in volume by 2.8% compared to control flies. In wild-type animals, increasing the density at which larvae are reared results in an increase in the volume of the calyx in the adult brain. This plasticity is still seen in rut1 mutants.
Hemizygous males show increased sensitivity to ethanol in an inebriometer assay. The ethanol-sensitive phenotype is reversed by treatment of the flies with forskolin (an adenylate cyclase activator).
After presentation of electric shock with a first odour, rut1 flies show a strongly reduced avoidance of a second, different odour compared to wild-type flies.
rut1 flies kept in constant darkness have a smaller lamina volume than rut1 flies kept in constant light, as is also seen for wild-type flies.
Modulation of voltage gated K+ currents induced by the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP38) is eliminated. Application of cAMP analogs or forskolin is sufficient to restore PACAP38 enhancement of K+ currents.
Mutant diminishes cAMP synthesis and reduced the rate of habituation (using the jump-and-flight escape response). Habituation is extremely rapid in dnc rut double mutants.
Growth cone exploratory movement is nearly arrested. Growth cones become active when perfused with db-cAMP (dibutyryl cAMP). Motility is also restored by counterbalancing the effects in rut dnc double mutants.
Slightly reduced grooming behavior.
The voltage-activated transient K+ current (IA) in the larval muscle fibres of homozygotes is normal. The voltage-activated delayed K+ current (IK) in the larval muscle fibres of homozygotes is almost normal. The amplitude of the delayed plateau outward K+ current (IS) in the larval muscle fibres of rut1 animals is reduced to levels below that of wild-type if the fibres are treated with caffeine.
Mutation abolished catalytic activity.
Reduction in basal level of adult adenylate cyclase. Calcium insensitive.
Lack of PTP and reduced facilitation.
The anteronotopleural neuron responds to deflection of the bristle with a burst of action potentials, and shows adaptation in response to a sustained deflection towards the body wall. The sensory response to repetitive stimulation is independent of CNS feedback. The anteronotopleural neuron fatigues less than that of wild type.
Sex-dependent enhancement in pertussis toxin catalysed ADP-ribosylation with respect to wild type: attributed in part to an increase in the α subunit of the G0-like protein.