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General Information
Symbol
Dmel\Dysbe01028
Species
D. melanogaster
Name
FlyBase ID
FBal0161105
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dysb1, dysb1, pBace01028
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Insertion components
PBac{RB}Dysbe01028
Product class / Tool use(s)
Encoded product / tool
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Dysbe01028 homozygous wandering third instar larvae 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 Dysbe01028 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 Dysbe01028 presynaptic bouton endosomes as compared to both unstimulated mutants and stimulated wild-type controls, and a significant decrease in the density of Dysbe01028 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 Dysbe01028 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.

Dysbe01028 heterozygote third instar larvae do not show any defects in the number or size of boutons nor the axonal branching at neuromusclular junctions.

Dysbe01028 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 Dysbe01028 mutants. Heterozygous larvae also show reduced number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons.

Wild-type synapses increase their quantal content following Phillanthatoxin-433 (PhTx-433) treatment. In contrast, Dysbe01028 animals do not display a homeostatic increase in quantal content.

Dysbe01028 has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. mEJP amplitude is not altered in these flies. Homozygous Dysbe01028 mutant flies fail to show the increase in quantal content normally observed in response to philanotoxin, and this phenotype is not seen in heterozygotes. The rate of vesicle depletion at both low and high frequency stimulation is similar to controls.

Expression of DysbScer\UAS.cDa under the control of Scer\GAL4elav-C155 in a Dysbe01028/+ mutant background has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls.

Homozygous Dysbe01028 mutant flies exhibit deficits in short term olfactory habituation. This phenotype is not observed in the heterozygote.

Dysbe01028/Df(3L)BSC416 mutant flies exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote.

Dysbe01028 heterozygotes do not exhibit defects in synaptic homeostasis.

Homozygous dysbe01028 mutant larvae show significantly attenuated excitatory junctional currents in the neuromuscular junction compared to controls. This attenuation is seen at various calcium concentrations and without significant morphological changes.

The dopamine concentration in dysbe01028 mutant heads is around twofold of that in wild type cells.

Homozygous dysbe01028 mutant adult flies exhibit defects in memory retention following exposure to an odor previously associated without electric shock. Memory is affected at both 1h and 3h after single session training and 24 hours after repetitive training. The sensorimotor responses necessary for performing the learning task are not altered. This phenotype can be rescued by feeding flies with the NMDA receptor agonist, glycine.

dysbe01028 mutant flies show elevated activity in response to light taps on the container compared to wild type flies of the same age. This hyperactivity can be significantly rescued by feeding flies resperine or α-methyl-p-tyrosine (AMPT).

dysbe01028 mutant flies do not exhibit the strong wild type bias towards females, courting male flies as well as female flies. No phenotypes are seen in either of the single heterozygotes. This phenotype can be significantly rescued by feeding flies resperine or α-methyl-p-tyrosine (AMPT).

Homozygous and dysbe01028/Df(3L)BSC416 neuromuscular junctions show a complete absence of homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.

Bouton number and active zone density at the neuromuscular junction are normal in mutant larvae.

Homozygous larvae show no significant change in baseline synaptic transmission in 0.5mM extracellular Ca[2+] compared to controls. However, at reduced extracellular Ca[2+] (0.2 to 0.4mM) , baseline synaptic transmission is significantly impaired in the mutants relative to controls. At reduced extracellular Ca[2+] both paired-pulse facilitation and facilitation that occurs during a prolonged stimulus train are increased in the mutants.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference

CG6856[+]/Dysbe01028 is a non-enhancer of neurophysiology defective | dominant phenotype of cacS

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Dysb[+]/Dysbe01028 is a suppressor of NMJ bouton | supernumerary phenotype of Blos1EY06269

Dysb[+]/Dysbe01028 is a suppressor of NMJ bouton | supernumerary phenotype of Blos1ex65

Additional Comments
Genetic Interactions
Statement
Reference

The expression of PldnScer\UAS.cCa 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 Dysbe01028 homozygous wandering third instar larvae; homozygosity for Dysbe01028 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 reduced number of dendritic branches as well as the total dendrite length in class IV dendritic arborizing neurons characteristic for Dysbe01028 heterozugous larvae is not modified by combination with a single copy of Arpc1Q25sd.

Presynaptic expression of comtScer\UAS.T:Zzzz\FLAG using Scer\GAL4elav-C155 restores the homeostatic quantal content increase to wild-type levels in Dysbe01028 mutants.

Blos1EY06269 Dysbe01028 double heterozygotes have no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. Synaptic vesicles are similar in size to controls. The increase in quantal content normally observed in response to philanotoxin is not seen. One copy of Dysbe01028 suppresses the dominant changes in mEJP amplitude and quantal content seen in Blos1EY06269/+ mutant NMJs. The increase in bouton number seen in Blos1EY06269/+ NMJs is also suppressed.

Expression of DysbScer\UAS.cDa under the control of Scer\GAL4elav-C155 in a Blos1EY06269/+; Dysbe01028/+ mutant background has no effect on excitatory junction potential (EJP) amplitude or miniature EJP frequency compared to controls. The mEJP amplitude is increased, similar to that seen in Blos1EY06269/+ mutant flies.

One copy of Dysbe01028 suppresses the dominant changes in mEJP amplitude and quantal content seen in Blos1ex65/+ mutant NMJs. The increase in bouton number seen in Blos1ex65/+ NMJs is also suppressed. Dysbe01028 Blos1ex65 double heterozygotes exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote alone.

Dysbe01028 Blos1ex2 double heterozygotes exhibit deficits in short term olfactory habituation. This phenotype is not observed in either heterozygote alone.

Dysbe01028 heterozygotes that are also heterozygous for Df(2L)Exel6277 (which removes the entire Snapin locus), exhibit significantly less homeostatic compensation compared with either heterozygous mutant alone. Co-expression of SnapinScer\UAS.cDa in motorneurons (under the control of Scer\GAL4VGlut-OK371) restores homeostasis towards control levels (although this rescue is not complete).

Double-heterozygous Syt1AD4/+ ; Dysbe01028/+ flies exhibit normal homeostatic compensation.

e1/dysbe01028 heteroallelic mutants display locomotor hyperactivity and mating disorientation (loss of the strong male bias towards the courtship of females).

GluRIIASP16 ; dysbe01028 double mutant larvae do not show homeostatic compensation at the neuromuscular junction.

The phenotype of reduced synaptic homeostasis at the neuromuscular junction after treatment with philanthotoxin-433 that is seen in cacS/+ larvae is not enhanced by dysbe01028/+.

Expression of cacScer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4elav-C155 does not restore homeostatic compensation at the neuromuscular junction in dysbe01028 larvae.

Xenogenetic Interactions
Statement
Reference

The neuromuscular junction bouton phenotype characteristic for third instar larvae expressing Hsap\DISC1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4tub.PU is enhanced by combination with a single copy of the Dysbe01028 allele: not only is the total bouton areas decreased further, in addition the total number of boutons as well as their individual size is significantly reduced compared to wild-type, whereas the number of axonal branching points remains normal.

Pan-neuronal expression of Hsap\DTNBP1Scer\UAS.cSa under the control of Scer\GAL4elav-C155 rescues the larval neuromuscular junction excitatory junctional current defects and the adult short term memory defects observed in dysbe01028 mutants.

Expression of Hsap\DTNBP1Scer\UAS.cSa in the glia under the control of Scer\GAL4repo partially suppresses the locomotor defects seen in dysbe01028 mutants. The increase in dopamine levels seen in dysbe01028 mutant heads is also suppressed.

Complementation and Rescue Data
Comments

The expression of DysbScer\UAS.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4RapGAP1-OK6 partially 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 junction exhibited by Dysbe01028 homozygous wandering third instar larvae.

The increased number of boutons on neuromuscular junctions observed in Dysbe01028/+ heterozygous third instar larvae is suppressed by expression of DysbScer\UAS.T:Avic\GFP-YFP.Venus under the control of Scer\GAL4elav-C155 in the mutant background.

Presynaptic expression of DysbScer\UAS.cDa using Scer\GAL4elav-C155 restores the homeostatic quantal content increase to wild-type levels in Dysbe01028 mutants.

Expression of dysbScer\UAS.cSa under the control of Scer\GAL4elav-C155 rescues the attenuated excitatory junctional currents recorded in the larval neuromuscular junction in dysbe01028 mutants. The short term memory defects are also rescued. The locomotor and mating disorientation phenotypes are not rescued, nor is the dopamine level in dysbe01028 mutant heads.

Expression of dysbScer\UAS.cSa in glia under the control of Scer\GAL4repo fails to rescue the short term memory defects seen in dysbe01028 mutant flies. However, glial expression of dysbScer\UAS.cSa is able to rescue the locomotor and mating disorientation phenotypes. The increased dopamine levels in the head are also rescued.

Expression of dysbScer\UAS.cSa in glutamatergic neurons under the control of Scer\GAL4VGlut-OK371 rescues the short-term memory defects seen in dysbe01028 mutant flies.

Acute expression of dysbScer\UAS.cSa under the control of Scer\GAL4hs.PU rescues the short-term memory defects and mating disorientation seen in dysbe01028 mutant flies. The increase in dopamine levels seen in dysbe01028 mutant heads is also suppressed.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (13)