P-element mutagenesis using the SynP1+P2 strain containing the P{lacW}SynP1 and P{lacW}SynP2 insertions has resulted in precise excision of the P{lacW}SynP2 insertion together with an imprecise excision of the P{lacW}SynP1 insertion. The imprecise excision results in the deletion of 1397bp around the original insertion site. The deletion eliminates 349bp of the presumed promoter region including the putative transcription start site, the first known exon (207bp) and 841bp of the first intron, while the coding region remains unaffected.
A precise excision of the P{lacW}SynP2 insertion present in the SynP1+P2 mutant, together with a 1.5kb deletion around the P{lacW}SynP1 insertion present in the SynP1+P2 mutant, eliminating the promoter and the first exon of the Syn gene.
Reported as a 1397bp deletion, which removes 349bp of untranstlated sequences, the 207bp first exon, and 841bp of the first intron.
Syn97 mutant third instar larvae do not display any abnormalities in the pattern or duration of peristaltic wave contractions and adult survival rate is comparable to controls.
Syn97 mutants exhibit a significant reduction in the number of 'ghost' boutons (lacking postsynaptic specializations in resting and high-K[+]-stimulated preparations).
K[+]-stimulated growth in Syn97 larvae is reduced by approximately 60%.
Syn97 mutants do not exhibit defects in the number of synaptic boutons per neuromuscular junction in the 3rd instar larval stage.
Synaptic vesicle depletion in Syn97 synapses may be the result of their impaired growth and development.
In wild-type flies, forskolin pretreatment of neuromuscular junctions significantly promotes activity-dependent synaptic growth. This effect is completely abolished in Syn97 mutants.
Syn97 homozygote adult flies are seizure-prone (their seizure behavior includes hyperactivity resulting in flies flipping on their backs) and show significantly longer recovery times in a modified bang-sensitivity assay.
Syn97 larvae show a 50% reduction in an odor-sugar associative learning paradigm, while are still able to taste, smell and move. Susceptibility to stress and olfactory adaptation are unchanged.
Mutants show no obvious anatomical defects in the synaptic neuropil of the adult brain.
The number and ultrastructure of synaptic boutons at the neuroumuscular junction of muscles 12/13 and 6/7 is not significantly different in mutant larvae compared to wild type.
The mean excitatory junction potential (EJP) amplitude at 0.5Hz stimulus frequency and the spontaneous miniature EJP amplitude and frequency at the mutant larval neuromuscular junction are normal.
Wing beat frequency during tethered flight is significantly increased in mutant flies compared to controls. Mutant flies show increased walking activity compared to controls, with a significant difference in the early phase (60-120 minutes) but not in the late phase of activity.
Optomotor responses of mutant flies are normal at low pattern speeds. However, fast moving patterns are followed significantly more efficiently by the mutant flies than by wild-type flies.
Mutant flies habituate significantly faster than mutant flies in an olfactory jump assay in response to repeated benzaldehyde odour exposure.
Mutant flies show a significantly higher ethanol tolerance than wild-type flies in an inebriometer assay.
Mutant flies are slightly but significantly impaired in heat avoidance during training in the heat-box paradigm for place learning.
Mutant flies perform significantly poorer than wild-type in a 3-minute memory test in an olfactory associative learning assay.
Mutant male flies without mating experience court mated females significantly less persistently than do wild-type males during a 20-minute period. Like wild-type males, the mutant males stop courting males at the end of this period, demonstrating their ability to learn. However, after 30 and 180 minutes in isolation, the mutant males are significantly more likely than wild-type males to resume courting mated females during a 5-minute exposure, indicating a defect in memory.
Syn97 is rescued by Scer\GAL4elav-C155/SynUAS.cVa
Syn97 is rescued by Scer\GAL4elav-C155/Syn1-12.UAS
Syn97 is rescued by Scer\GAL4elav-C155/Syn1-12.UAS/Scer\GAL80ts.αTub84B
Syn97 is rescued by Scer\GAL4Mef2.247/Syn1-12.UAS
Syn97 is not rescued by Syn1-12.UAS/Scer\GAL4GH146
Syn97 is not rescued by Syn1-12.UAS/Scer\GAL4NP0225
Syn97 is not rescued by Scer\GAL4elav-C155/SynPKA-AA.UAS
The addition of SynScer\UAS.cVa (under the control of Scer\GAL4elav-C155) to a Syn97 mutant background rescues the 'ghost' bouton phenotype, but does not promote futher (over)growth.
Pan-neuronal expression of Syn1-12.Scer\UAS, under the control of Scer\GAL4elav-C155 fully rescues associative learning in Syn97 mutants.
Pan-neuronal acute expression of Syn1-12.Scer\UAS, through heat-shocking of flies carrying Scer\GAL80ts.αTub84B as well as Scer\GAL4elav-C155 (where Scer\GAL80ts.αTub84B blocks expression until heat-shock), fully rescues the associative odor-sugar learning in Syn97 mutants.
Expression of Syn1-12.Scer\UAS in the mushroom bodies, under the control of Scer\GAL80Mef2.PT, fully rescues the associative odor-sugar learning in Syn97 mutants.
Expression of Syn1-12.Scer\UAS in the projection neurons, under the control of either Scer\GAL4GH146 or Scer\GAL4NP0225, fails to rescue the associative odor-sugar learning in Syn97 mutants.
Pan-neuronal expression of Syn1-12.Scer\UAS, under the control of Scer\GAL4elav-C155 fails to rescue the associative learning defects found in Syn97 mutants.