FLPase-mediated recombination between PBac{WH}Pldnf05716 and PBac{WH}Sugbf05753 results in deletion within Pldn (bases 11,689,565 to 11,691,527 on chromosome 3L).
FLPase-mediated recombination between the progenitor insertions results in a deletion at 3L:11689565..11691527 .
The neuromuscular junctions of PldnΔ1 homozygous or PldnΔ1/Df(3L)BSC675 transheterozygous wandering third instar larvae present no obvious differences in the morphology and structure of synapses, as shown by the absence of significant differences in the number of presynaptic boutons, in the presynaptic membrane area, and in the number and density of presynaptic active zones, as compared to controls.
PldnΔ1 homozygous or PldnΔ1/Df(3L)BSC675 transheterozygous wandering third instar larvae exhibit no obvious defects in neurotransmission across the neuromuscular junction, as shown by the absence of significant differences in the frequency and amplitude of spontaneous miniature excitatory postsynaptic potentials, in the amplitude of evoked excitatory postsynaptic potentials, in quantal content, in the frequency of asynchronous release and probability of release upon stimuli, in the cumulative excitatory postsynaptic current, and in the estimated size of the readily releasable vesicle pool, as compared to controls; PldnΔ1 homozygotes display a significantly increased rate of depletion and a significantly decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junction, as compared to controls.
Under rest conditions, the neuromuscular junction presynaptic boutons of PldnΔ1 homozygous wandering third instar larvae show no significant differences in the size and density of endosomes, in the intensity of presynaptic T-bars, in the size, number and density of synaptic vesicles, and in the density of tubular endosomes, but show a significant increase in the density of cisternal endosomes, as compared to controls. Stimulation with 90mM potassium chloride leads to a significant decrease in the size and density of PldnΔ1 presynaptic bouton endosomes as compared to both unstimulated mutants and stimulated wild-type controls, and a significant decrease in the density of PldnΔ1 presynaptic bouton vesicles as compared to unstimulated mutants but not to stimulated wild-type controls, whereas this stimulation has no significant effect either in the size and density of endosomes or in the density of synaptic vesicles in wild-type presynaptic boutons; stimulation with potassium chloride also leads to the density of cisternal endosomes and tubular endosomes in PldnΔ1 presynaptic boutons to be significantly decreased and increased, respectively, as compared to both unstimulated mutants and stimulated wild-type controls, whereas this stimulation leads to a significant increase in the density of cisternal endosomes, but not tubular endosomes, in wild-type presynaptic bouton endosomes.
Pldndel homozygous as well as heterozygous mutant third instar larvae display increased number of boutons on neuromuscular junctions compared to controls, but not when the larvae are kept on 'DD' food (after Dickman and Davis, 2009) as it induces higher number of boutons in the control flies and this is not elevated further in Pldndel mutants.
PldnΔ1 has abnormal neurophysiology | wandering third instar larval stage | conditional phenotype, non-suppressible by DysbUAS.Venus/Scer\GAL4RapGAP1-OK6
PldnΔ1/PldnΔ1 is a non-enhancer of abnormal neurophysiology | wandering third instar larval stage phenotype of GluRIIASP16
Pldn[+]/PldnΔ1 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Arpc1Q25sd
PldnΔ1/PldnΔ1 is a non-suppressor of abnormal neurophysiology | wandering third instar larval stage phenotype of GluRIIASP16
PldnΔ1 has synapse | wandering third instar larval stage | conditional phenotype, non-suppressible by DysbUAS.Venus/Scer\GAL4RapGAP1-OK6
PldnΔ1/PldnΔ1 is a non-enhancer of synapse | wandering third instar larval stage phenotype of GluRIIASP16
Pldn[+]/PldnΔ1 is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of Arpc1Q25sd
PldnΔ1/PldnΔ1 is a non-suppressor of synapse | wandering third instar larval stage phenotype of GluRIIASP16
PldnΔ1 homozygosity does not significantly affect the decreased amplitude of spontaneous miniature excitatory postsynaptic potentials, the increased quantal content, or the amplitude of evoked excitatory postsynaptic potentials exhibited during the neurotransmission across the neuromuscular junctions of GluRIIASP16 homozygous wandering third instar larvae; homozygosity for PldnΔ1 also does not significantly affect the total quanta release during neurotransmission across shi1 homozygous wandering third instar larval neuromuscular junctions at the restrictive 32[o]C temperature.
The increased number of boutons on neuromuscular junctions observed in third instar larvae mutant for any of the following alleles: Arpc1Q25sd (in heterozygous state), Pldndel (homozygous) or Dysbe01028 (either homozygous or heterozygous) is restored to wild-type levels in both Arpc1Q25sd/+;Pldndel/+ and Arpc1Q25sd/+;Dysbe01028/+ double heterozygotes.
The expression of DysbScer\UAS.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4RapGAP1-OK6 does not suppress either the increased rate of depletion or the decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junction exhibited by PldnΔ1 homozygous wandering third instar larvae.
PldnΔ1 is rescued by Scer\GAL4RapGAP1-OK6/PldnUAS.cCa
The expression of PldnScer\UAS.cCa under the control of Scer\GAL4RapGAP1-OK6 suppresses both the increased rate of depletion and the decreased rate of recovery of the synaptic vesicle pool upon high-frequency stimulation of the neuromuscular junctions of PldnΔ1 homozygous wandering third instar larvae.
