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General Information
Symbol
Dmel\Hsc70-4Δ19
Species
D. melanogaster
Name
FlyBase ID
FBal0124177
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
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

Contains a large deletion internal to the P{PZ}Hsc70-403550 insertion.

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 ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Hsc70-4Δ19/Df(3R)BSC471 larvae show a significant decrease in endosomal microautophagy at the neuromuscular junction compared to wild-type controls. Macroautophagy, synaptic vesicle endocytosis and proteasomal activity are not significantly different from wild type. Ultrastructurally, the boutons show no significant difference to wild type.

The mean excitatory junctional current (EJC) amplitude at the neuromuscular junction is significantly lower than wild type in Hsc70-4Δ19/Df(3R)BSC471 larvae.

Mutant neuromuscular junctions show reliable homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.

Homozygous larvae show sporadic but reduced muscle contractions. The nerve-evoked excitatory junctional potential (EJP) amplitudes in homozygous mutant larvae or in Hsc70-4Δ19/Hsc70-4Δ11 or Hsc70-4Δ19/Hsc70-4Δ356 transheterozygotes are reduced to about half that of controls. EJP amplitudes are not reduced by a fatigue of evoked release, because responses sequentially recorded at 0.2 Hz do not progressively diminish. Evoked but not spontaneous synaptic transmission is thermo-intolerant in mutants. After increasing the temperature from 23oC to 30oC, homozygous mutants show a complete loss of EJP amplitudes after 20 minutes when stimulated at 0.2 Hz.After cooling to 23oC, at least a partial recovery of EJPs is always observed within 11 minutes. At a normal electrotonic stimulation intensity, application of Tetrodotoxin abolishes nerve-evoked EJPs in mutants as in wild-type. Subsequent stimulation with intensities 10 fold over threshold then elicit EJPs both in mutants and wild-type. However such electrotonically elicited EJPs are still reduced in mutants to about half that of controls, thus indicating a defect downstream of nerve excitation. Analysis of spontaneous neurotransmitter release reveals no postsynaptic defects at mutant neuromuscular junctions (NMJs). Mutant NMJs also have no abnormalities in their gross morphology. The quantal content of evoked release in homozygotes and Hsc70-4Δ19/Hsc70-4Δ11 or Hsc70-4Δ19/Hsc70-4Δ356 transheterozygotes is reduced to a third to a half of control. The estimated quantal content in homozygotes is significantly reduced for each examined Ca<up>2+</up>e compared to controls. Nerve evoked cytosolic Ca2+ levels during stimulation attain similar or higher values in homozygous mutants than in control boutons. The loss in neurotransmitter release in mutants is caused by a defect in exocytosis downstream of ca2+ entry. Synaptic vesicle recycling at mutant NMJs is normal. Ultrastructural studies of 3rd instar larval NMJs show that mutant terminals contain a large number of clear synaptic vesicles similar to controls. As in controls clathrin coated vesicles are not detectable. During repetitive stimulation, the evoked release are not depressed, suggesting that the number of releasable vesicles does not limit exocytosis in homozygous mutants. Increasing amounts of external and internal (residual) Ca2+ counteract a reduced probability of vesicle fusion in mutants caused by a decreased sensitivity of the Ca2+ signalling pathway triggering function.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Sgt56 ; Hsc70-4Δ19/Df(3R)BSC471 double mutant larvae show the same decreased level of endosomal microautophagy and significant decrease in mean excitatory junctional current amplitude at the neuromuscular junction as seen in Hsc70-4Δ19/Df(3R)BSC471 single mutants.

The increase in the number of multivesicular bodies (MVBs) and in the number of intraluminal vesicles per MVB area seen at the neuromuscular junction in Sgt56 larvae is suppressed in Sgt56 ; Hsc70-4Δ19/Df(3R)BSC471 double mutant larvae.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of either Hsc70-4wt.T:Ivir\HA1 or Hsc70-4D10N.T:Ivir\HA1 completely rescues the decrease in endosomal microautophagy which is seen at the neuromuscular junction in Hsc70-4Δ19/Df(3R)BSC471 larvae.

Expression of Hsc70-43KA.T:Ivir\HA1 fails to rescue the decrease in endosomal microautophagy which is seen at the neuromuscular junction in Hsc70-4Δ19/Df(3R)BSC471 larvae.

Expression of Hsc70-4wt.T:Ivir\HA1 completely rescues the decrease in mean excitatory junctional current amplitude which is seen at the neuromuscular junction in Hsc70-4Δ19/Df(3R)BSC471 larvae.

Expression of either Hsc70-43KA.T:Ivir\HA1 or Hsc70-4D10N.T:Ivir\HA1 does not rescue the decrease in mean excitatory junctional current amplitude which is seen at the neuromuscular junction in Hsc70-4Δ19/Df(3R)BSC471 larvae.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Hsc70-4Δ19
Name Synonyms
Secondary FlyBase IDs
    References (3)