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General Information
Symbol
Dmel\Dscam105518
Species
D. melanogaster
Name
FlyBase ID
FBal0008092
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DscamP1, dscam1p, Dscamp
Key Links
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

The insertion is beyond exon 4 of the Dscam gene.

Insertion components
P{PZ}Dscam105518
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Dscam105518 homozygous embryonic heart cardioblasts show significant decreases in filopodial and lamellopodial activities, but not in migration velocity, as compared to controls. Dscam11 heterozygous embryonic heart cardioblasts also show a significant decrease in filopodial activity, but not in lamellopodial activity or migration velocity, as compared to controls.

Dscam105518 mutant DL1 olfactory projection neuron clones exhibit loss of dorsal branches in axons. There is no increase in the number of dendrites spilling-over to the outside of the antennal lobe compared to wild type.

Generation of Dscam105518 mutant mushroom body clones causes loss of the β lobe.

Single C4 da neurons homozygous for Dscam105518, exhibit markedly reduced presynaptic arbor growth.

Levels of apoptosis are not increased in the thoracic and abdominal segments of the Dscam05518 mutant ventral nerve cord.

27.5% of homozygous Dscam05518 embryos show defects in axon guidance in the Bolwig's nerve.

30% of segments fail to separate the anterior and posterior commissures correctly in Dscam05518 embryos.

About 5% of heterozygotes exhibit some Bolwig's nerve targeting defects. Dscam05518 hemizygous mutants exhibit mild to severe disorganisation of embryonic axon tracts. Breaks in the connectives, predominantly of the outer two fascicles are observed. In addition axon bundles aberrantly cross the midline. Some 53%-58% of Bolwig's nerve (BN) projections are defective in Dscam1/Df(2R)cos-2 hemizygotes. In half of the "abnormal projections" the entire nerve mistargets, whereas in the remainder only a subset of axons does. Many otherwise normal projections show abnormal expansion of BN terminus at P2. These phenotypes are 53-58% penetrant.

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

Dscam105518/Dscam1[+] is a non-enhancer of filopodium | embryonic stage phenotype of robo11

Dscam105518/Dscam1[+] is a non-enhancer of lamellipodium | embryonic stage phenotype of robo11

Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Dscam105518, robo11 double heterozygotes show a similar decrease in filopodial and lamellopodial activities compared to either single heterozygote conditions, and show no significant changes in migration velocity compared to wild-type controls.

Dscam105518 DL1 projection neuron mutant clones generated in a TBCD1/+ background have an increased number of dendrites that spill over to the outside of the antennal lobe compared to wild type clones in a TBCD1/+ mutant background. The loss of the dorsal branch seen in Dscam105518 mutant clones alone is not enhanced in a TBCD1 mutant background.

Dscam05518 fra4 double mutants show a significant increase in apoptosis in the thoracic and abdominal segments of the ventral nerve cord compared to controls.

67% of Dscam05518/Dscam05518 fra4/fra4 embryos show defects in axon guidance in the Bolwig's nerve.

The penetrance of the axon guidance defect phenotype that is seen in the Bolwig's nerve of Dscam05518/Dscam05518 fra4/fra4 double mutant embryos is not increased by addition of Dscam3c02826/Dscam3c02826.

22.5% of Dscam05518/+ ; fra4/+ embryos show defects in axon guidance in the Bolwig's nerve.

38% of Df(1)NP5/+ ; Dscam05518/+ embryos show defects in axon guidance in the Bolwig's nerve.

34% of Df(1)NetABΔ/+ ; Dscam05518/+ embryos show defects in axon guidance in the Bolwig's nerve.

84% of segments fail to separate the anterior and posterior commissures correctly in Dscam05518 Dscam3c02826 embryos.

Dscam05518 fra4 embryos show defects in the commissures of the central nervous system; 9% of anterior commissures are absent, 24% of anterior commissures are thin, 5% of posterior commissures are absent and 39% of posterior commissures are thin. 51% of segments fail to separate the anterior and posterior commissures correctly.

Dscam05518 Abl4 embryos show defects in the commissures of the central nervous system; 23% of anterior commissures are absent, 33% of anterior commissures are thin, 65% of posterior commissures are absent and 26% of posterior commissures are thin. 19% of segments fail to separate the anterior and posterior commissures correctly.

Dscam05518 fra4 Dscam3c02826 embryos show defects in the commissures of the central nervous system; 39% of anterior commissures are absent, 51% of anterior commissures are thin, 36% of posterior commissures are absent and 55% of posterior commissures are thin. 5% of segments fail to separate the anterior and posterior commissures correctly.

Dscam05518 fra4 Abl4 embryos show defects in the commissures of the central nervous system; 98% of anterior commissures are absent, 2% of anterior commissures are thin and 100% of posterior commissures are absent.

The severity of the SP1 axon midline crossing defects seen in fraunspecified embryos is enhanced in fraunspecified Dscam05518 Dscam3c02826 triple mutants.

37% of EG axon bundles are thin or absent in Dscam05518 fraunspecified mutant embryos.

About 42% of Dscam05518/dock3 embryos exhibit some Bolwig's nerve targeting defects. About 38% of Dscam05518/Pak6 embryos exhibit some Bolwig's nerve targeting defects.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Rescued by
Comments

The dramatic reduction in presynaptic arbor growth in Dscam105518 mutants is rescued by expression of Dscam1+t73.3.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Complements: l(2)43Bb04614a. Complements: cosk16101. Complements: cosk16122.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (12)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (17)