|Feature type||allele||Associated gene||Dmel\Syx1A|
|Also Known As||syx3-69|
|Map ( GBrowse )|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Amino acid replacement: T254I.
Nucleotide substitution: C?T.
Amino acid replacement: T254I. Nucleotide substitution: C?T. The T254I mutation lies in the 'a' position on the hydrophobic face of a heptad repeat at the end of the third coiled coil motif of the Syx1A protein, the H3 domain, three amino acids upstream of the C.botulinum C cleavage site.
neurophysiology defective | heat sensitive (with Syx1AΔ229), with Scer\GAL4elav-C155, Syx1AScer\UAS.cBa
|Phenotype Manifest In|
optic cartridge & synaptic vesicle
Syx1A[3-69] homozygous mutants show similar levels of synaptic vesicle endocytosis at the larval neuromuscular junction compared to control animals at both 25[o]C and 37[o]C.
Syx1A3-69 mutant flies are rapidly paralysed at 38oC but recover within 3 minutes when returned to a permissive temperature after a 20 minute period of paralysis. While Syx1A3-69 mutant flies are paralysed at 38oC, they are not motionless, they constantly shake their legs and abdomens. Repetitive and phase-locked leg shaking is easily observed in Syx1A3-69 flies at both the permissive temperature (20oC) and the restrictive temperature (38oC) following artificial stimulus of the giant fiber neuron. The synaptic response of the dorsal longitudinal indirect flight muscles from Syx1A3-69 flies is maintained at 38oC. During observations, the intracellular electrodes are often dislodged from the dorsal longitudinal indirect flight muscles only from Syx1A3-69 flies, along with a high incidence of spontaneous action potentials in the mutant muscles, indicating that synaptic transmission is not blocked at restrictive temperatures in Syx1A3-69 flies. Light-induced 'on' and 'off' transient potentials of electroretinograms are not blocked by exposure of the Syx1A3-69 fly to the restrictive temperature. In fact, the 'on' transient potential is slightly increased in amplitude at 38oC. The average amount of 7S SNARE complex is significantly increased in Syx1A3-69 mutants compared to wild-type, at 22oC. Similarly, the level of SNARE multimers is also significantly increased in the mutant. The frequency of constitutive (or spontaneous) release of miniature excitatory postsynaptic potentials (mEPSPs) from third instar larval body-wall muscles innervated by motoneurons is dramatically increased some 7-fold in Syx1A3-69 flies, compared to the wild-type. The average mini amplitude is similar in both the Syx1A3-69 mutant and the wild-type larvae, suggesting that quanta and postsynaptic receptors likely remain normal. The unusually high rate of spontaneous release remains in the Syx1A3-69 mutant in the absence of extracellualr Ca2+, although the resting potential is no different to wild-type. The mini frequency remains 13-fold higher in Syx1A3-69 mutants compared to the wild-type in Ca2+-free saline containing the membrane-permeable Ca2+ chelator EGTA-AM. The amplitude of evoked EPSPs is significantly increased to 37mV in the Syx1A3-69 mutant from 25mV in the wild-type. Because the average mini amplitude is not significantly different between the mutant and the wild-type, this increase in EPSP amplitude most likely reflects an enhancement in presynaptic release. There is a 2-fold increase in quantal content in the mutant compared to the wild-type. Syx1A3-69 mutants do no exhibit a detectable difference in synaptic vesicle recycling compared to wild-type. The resting potential of the muscle fiber in Syx1A3-69/+ and Syx1A3-69/Syx1A3-69 mutants is not significantly different from that in the wild-type. In Syx1A3-69/+ mutants the frequency of spontaneous fusion is significantly higher than that in the wild-type, but much lower than that in the homozygote. The amplitude of evoked EPSPs in Syx1A3-69/+ mutants is similar to that in homozygotes, but significantly higher than that in the wild-type. In Syx1A3-69/Syx1AΔ229 mutants, the mini-frequency is 22.3Hz, which is significantly higher than in the wild-type larvae. At 0.8mM Ca2+, the evoked EPSP amplitude is significantly increased to 37.9mV from 29.5mV in the wild-type larvae. These results are similar to those found in Syx1A3-69 homozygotes. Neuronal expression of Syx1AScer\UAS.cBa under the control of Scer\GAL4elav-C155 in Syx1A3-69/Syx1AΔ229 results in a dramatic reduction in the frequency of constitutive secretion to 8.8Hz from 24.9Hz. The average amplitude of EPSPs is also significantly reduced in Syx1A3-69/Syx1AΔ229 mutants expressing Syx1AScer\UAS.cBa under the control of Scer\GAL4elav-C155. This EPSP amplitude is similar to that in Syx1AScer\UAS.cBa/Scer\GAL4elav-C155 flies, but significantly higher than wild-type.
After 10 minutes at 33oC, Syx1A3-69 homozygotes display only approximately 10% paralysis. Paralysed Syx1A3-69 flies completely recover to an upright position within 1-2 minutes after returning to room temperature.
Heterozygous flies lose coordination as the temperature is raised, such that at 39oC, they display a "bottom-dwelling" phenotype when placed in glass test tubes, in contrast to wild-type flies at this temperature, which are able to run up and down the sides of the tube for several minutes before also becoming uncoordinated. Homozygotes "pass out" completely in seconds at 39oC.
In ERG assay, mutants lose the on/off transients at 38oC. Recovery of transients at 20oC is rapid. Paralysis occurs after temperature shift to 38oC. Kinetics of onset of paralysis are quicker for homozygotes than for heterozygotes. ERG phenotypes correlate with paralytic phenotypes: time course of paralysis and recovery for Syx1A mutants is more rapid than for comt mutants. Ultrastructural studies reveal that the number of synaptic vesicles in photoreceptor terminals in the optic cartridge is dramatically increased. Clear increases occur in the number of vesicles clustered round T-bars. Number of docked vesicles is increased compared to wild type.
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by Act42A[+]/Act42AEP2096/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by aopEP598/aop[+]/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by CG3760EP548/CG3760[+]/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by CG9894[+]/BaccEP7/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by EP2[+]/EP2EP2/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by EP454[+]/EP454EP454/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by EP704EP704/EP704[+]/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by EP718[+]/EP718EP718/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by EP1244EP1244/Scer\GAL4[-]/EP1244[+]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by Etl1EP701/CG5899[+]/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by GmdEP315/Scer\GAL4[-]/Gmd[+]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by kisEP563/kis[+]/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by MESR4[+]/Scer\GAL4[-]/MESR4EP386
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by Pdk[+]/PdkEP547/Scer\GAL4[-]
Syx1A3-69 has uncoordinated | dominant | heat sensitive phenotype, suppressible by RpS23[+]/RpS23EP638/Scer\GAL4[-]
|Phenotype Manifest In|
Syx1A3-69, stmA1 has garland cell | wandering third instar larval stage | temperature conditional phenotype
stmA; Syx1A[3-69] double mutants show a strong reduction in synaptic vesicle endocytosis at the larval neuromuscular junction compared to control animals at both 25[o]C and 37[o]C. stmA; Syx1A[3-69] double mutants show endocytosis activity in garland cells at 25[o]C. At 37[o]C no endocytosis is observed.
stmA1; Syx1A3-69 double mutants rapidly paralyse at 33oC, with approximately 90% of mutants completely paralysed within 10 minutes. Approximately 5 minutes are required for all paralysed stmA1; Syx1A3-69 double mutants to regain an upright position after return to room temperature. stmA1/stmA1; Syx1A3-69/Syx1A3-69 homozygotes and stmA1/stmArev499; Syx1A3-69/Syx1A3-69 double mutants exhibit an indistinguishable synergistic genetic interaction.
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 5 )|
|Secondary FlyBase IDs|
|References ( 7 )|