Imprecise excision of the P{lacW} element, removing much of exon 1 (including the start codon), and all of exons 2, 3 and 4.
n-syb14/n-sybΔF33B third instar larvae have a normal number of varicosities at the neuromuscular junction of muscle fibres 6 and 7 and synaptic proliferation at the neuromuscular junction is normal.
Mosaic animals in which the eyes are made homozygous for n-sybΔF33B have eyes which are externally indistinguishable from those of controls, however, the on and off transients of the electroretinogram are absent in these flies. No evoked responses are observed at the neuromuscular junction in n-sybΔF33B larvae.
Excitatory synaptic currents (ESCs) are detected in mutant embryos, but virtually no large-amplitude ESCs characteristic of nerve-evoked ESCs are seen. Tetrodotoxin has no effect on the frequency or amplitude of ESCs (in contrast to wild type) and no evoked ESCs are elicited by nerve stimulation.
A reduction is seen in EJCs in n-sybΔF33B/n-sybI18 larvae over a full range of Ca2+ concentrations. Sensitivity to Calcium is not altered. There are no differences in mEJC amplitude that can explain the observed reduction in synaptic transmission. A reduction in Ca2+ cooperativity of synaptic transmission is seen. The mean mEJC decay time is not affected.
The frequency of miniature excitatory synaptic currents (mESCs) in high K+ saline increases in a Ca2+-dependent manner in mutant larvae.
The longitudinal tracts of the ventral nervous system, the motor nerves and the terminals of the motor neurons appear normal in homozygous embryos. Stimulation of the ventral ganglion fails to elicit any evoked current in the muscle in homozygous embryos, in contrast to wild-type. The frequency of miniature excitatory synaptic currents at the neuromuscular junction is reduced by approximately 75% in homozygous embryos compared to wild-type, although their mean amplitude is similar to that in wild-type embryos. Transheterozygotes with n-sybI4 or n-sybI18 can survive to adulthood, but the flies are very sluggish and often remain motionless for minutes at a time.
nSybΔF33B has abnormal neurophysiology phenotype, suppressible by Sybhs.PB
nSybΔF33B has abnormal neurophysiology | somatic clone phenotype, suppressible by Sybhs.PB
nSybΔF33B has neuromuscular junction phenotype, suppressible by Sybhs.PB
Scer\GAL4elav-C155-driven expression of nSybK83A.UAS in the nSybΔF33B background leads to reduced frequency of mESPCs at the larval NMJ compared to the rescue line expressing nSybUAS.cLa but the amplitude as well as area of the evoked excitatory postsynaptic currents is comparable in both lines.
The on and off transients of the electroretinogram are restored in mosaic animals in which the eyes are homozygous for n-sybΔF33B if they are also expressing Sybhs.PB. Evoked responses at the n-sybΔF33B neuromuscular junction are partially restored by expression of Sybhs.PB.
In Mhc1 ; n-sybΔF33B double mutants, Co2+ completely blocks the effect of forskolin on mSC frequency in larval neuromuscular junctions.
nSybΔF33B is rescued by nSyb+tCH322-83G13
Evoked responses at the n-sybΔF33B neuromuscular junction are partially restored by expression of n-sybhs.PB.
Selected as: Lethal in combination with n-sybF33.
Shows normal GABA staining in stage 17 nerve cord.