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General Information
Symbol
Dmel\Sdc10608
Species
D. melanogaster
Name
FlyBase ID
FBal0008157
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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
P{PZ}Sdc10608
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 ( 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

Homozygous larvae show a significant reduction in bouton number at the neuromuscular junction compared to wild type.

Sdc10608/Df(2R)48 larvae (carrying SaraUbi.PJ to provide Sara function) show a significant reduction in bouton number at the neuromuscular junction compared to wild type. Mean active zone area and number of active zones per bouton are normal.

The amplitude of the evoked excitatory junctional potential (EJP) is normal at the neuromuscular junction of Sdc10608/Df(2R)48 larvae (carrying SaraUbi.PJ to provide Sara function). The amplitude and frequency of miniature EJPs are not significantly different from normal.

Sdc10608 mutants display ISNb bypass at a similar rate to wild-type embryos.

Half of Df(2R)48/Sdc10608 larvae (in which Sara function has been rescued by SaraUbi.PJ) show photoreceptor projection and lamina-plexus defects. At the pupal level, these mutants show crossover of R7 axons between medullary cartridges and defective axon pathfinding to the medulla, with a low penetrance of R7/R8 terminal disruption. Electrophysiological analysis shows that as adults, these mutants have grossly abnormal ERGs, with defective photoreceptor polarization and complete absence of on- and off-transients.

Df(2R)48/Sdc10608 mutants (in which Sara function has been rescued by SaraUbi.PJ) have no rough eye phenotype and show no defects in the specification of photoreceptors, glia or lamina neurons.

Sdc10608 embryos show a high frequency of axons crossing the midline in the central nervous system.

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

Sdc10608/Sdc[+] is an enhancer of visible phenotype of DgdsRNA.UAS, Scer\GAL4Tub.PU

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Sdc10608/Sdc[+] is a suppressor of visible phenotype of DysdsRNA.C.UAS, Scer\GAL4Tub.PU

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

Sdc48/Sdc10608 is an enhancer of anterior fascicle & axon | ectopic phenotype of Lar5.5/Lar13.2

Sdc10608 is an enhancer of anterior fascicle & axon | ectopic phenotype of Larbypass

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

The commissural axon phenotype (failure to cross the midline) seen in embryos expressing Sema-1aScer\UAS.cYa under the control of Scer\GAL4P52 in a Sema-1ak13702 null background is not affected if the embryos are also heterozygous for Sdc10608.

Sema-1ak13702/+ ; Sdc10608/+ double heterozygous embryo do not show significant ISNb or SNa motor axon guidance defects compared to controls.

One copy of Sdc10608 moderately suppresses the detached posterior crossvein phenotype seen when DysdsRNA.NH2.Scer\UAS is expressed under the control of Scer\GAL4Act.PU but produces extra wing vein material.

One copy of Sdc10608 weakly suppresses the detached posterior crossvein phenotype seen when DysdsRNA.C.Scer\UAS is expressed under the control of Scer\GAL4tub.PU but produces extra wing vein material.

One copy of Sdc10608 enhances the posterior crossvein phenotype seen when DgdsRNA.Scer\UAS is expressed under the control of Scer\GAL4tub.PU.

Expression of dlpScer\UAS.cBa under the control of Scer\GAL4how-24B does not rescue the reduction in bouton number at the neuromuscular junction seen in homozygous Sdc10608 larvae.

Sdc10608 increases the penetrance of the Larbypass ISNb bypass phenotype by more than 2-fold. Sdc48/Sdc10608; Lar13.2/Lar5.5 (in which Sara has been rescued by expression of the SaraUbi.PJ transgene) mutants display an increased penetrance of the bypass phenotype (43% vs. 28%) relative to the corresponding Lar13.2/Lar5.5 transheterozygote.

Expression of dlpScer\UAS.T:Ivir\HA1, under the control of Scer\GAL4elav-C155, rescues the medulla patterning defects of Sdc10608/Df(2R)48 mutants (in which Sara function has been rescued by SaraUbi.PJ). However, this expression fails to rescue the ERG defects.

Xenogenetic Interactions
Statement
Reference

Sdc10608/Df(2R)48 third instar larvae (in which Sara function has been rescued by SaraUbi.PJ) have a decrease in the number of boutons per neuromuscular junction, compared to controls; this phenotype is rescued by expression of Sdc::Hsap\PDGFRBTM-Swap.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4how-24B.

Complementation and Rescue Data
Comments

Sdc10608/Df(2R)48 third instar larvae (in which Sara function has been rescued by SaraUbi.PJ) have a decrease in the number of boutons per neuromuscular junction, compared to controls; this phenotype is completely rescued by pre- (Scer\GAL4elav.PU) or post- (Scer\GAL4how-24B) synaptic expression of SdcScer\UAS.FL.T:Hsap\MYC, or pre- (and partial rescue with post-) synaptic expression of SdcScer\UAS.cJa; the phenotype is not rescued by expression of SdcΔCyto.Scer\UAS.T:Hsap\MYC, SdcΔC1.Scer\UAS.T:Hsap\MYC, SdcΔC2.Scer\UAS.T:Hsap\MYC or SdcΔEcto.Scer\UAS.T:Hsap\MYC driven by Scer\GAL4how-24B.

Expression of SdcScer\UAS.cJa under the control of Scer\GAL4elav.PU almost completely rescues the reduction in bouton number at the neuromuscular junction which is seen in Sdc10608/Df(2R)48 larvae (carrying SaraUbi.PJ to provide Sara function).

Expression of SdcScer\UAS.cJa under the control of Scer\GAL4how-24B provides limited rescue of the reduction in bouton number at the neuromuscular junction which is seen in homozygous Sdc10608 larvae.

Expression of SdcScer\UAS.cSa, under the control of Scer\GAL4elav-C155, rescues the medulla cartridge crossover and R7/R8 termini disruption pupal phenotypes of Df(2R)48/Sdc10608 mutants (in which Sara function has been rescued by SaraUbi.PJ). However, this expression fails to rescue photoreceptor projection defects to the larval lamina or ERG abnormalities in adults.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Complements: Fkbp1300734. Complements: MESK201467. Complements: domk08108. Complements: l(2)k10317k10317.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (16)