FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Dscam123
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General Information
Symbol
Dmel\Dscam123
Species
D. melanogaster
Name
FlyBase ID
FBal0148064
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Dscam23, Dscamnull
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

dendrite & abdominal dorsal/lateral multidendritic neuron | somatic clone | cell autonomous

dendrite & abdominal dorsal multidendritic neuron ddaA | somatic clone | cell autonomous

dendrite & abdominal dorsal multidendritic neuron ddaC | somatic clone | cell autonomous

dendrite & abdominal dorsal multidendritic neuron ddaD (with Dscam121)

dendrite & abdominal dorsal multidendritic neuron ddaD (with Dscam147)

dendrite & abdominal dorsal multidendritic neuron ddaD | somatic clone | cell autonomous

dendrite & abdominal dorsal multidendritic neuron ddaE (with Dscam121)

dendrite & dendritic arborising neuron | somatic clone | cell autonomous

Detailed Description
Statement
Reference

Dscam123/Dscam121 transheterozygous embryos show defects in dendritogenesis in the embryonic aCC motoneurons (misplacement of primary branches) compared to controls. No gross morphology defects are observed in the MP1 neurons at early embryonic stage.

Mutants show increased overlap and fasciculation of self-dendrites among dendritic arborization neurons in the larval body wall.

In DscamR496W/Dscam23 flies, the dorsal lobe nerve tract of the mushroom body does not form and the the medial lobe fails to extend to the midline. These phenotypes are 100% penetrant and exhibit similar but slightly weaker expressivity than Dscam23.

100% of DscamFRT/Dscam23 animals survive to late pupal stages.

Less than 25% of Dscam21/Dscam23 or DscamDf6055/Dscam23 larvae survive to late pupal stages.

Over 75% of Dscam3.31.8/Dscam23, Dscam10.27.25/Dscam23 and Dscam6.5.9/Dscam23 animals survive to late pupal stages.

Dscam21/Dscam23 embryos show defects in the organisation of the central nervous system, showing severely disrupted longitudinal tracts and some aberrant midline crossing.

Dscam3.31.8/Dscam23, Dscam10.27.25/Dscam23 and Dscam6.5.9/Dscam23 embryos show defects in the organisation of the central nervous system, showing disrupted longitudinal tracts.

Class I da neurons show defects in self-avoidance in Dscam21/Dscam23 larvae, such that in contrast to wild type, class I dendrites from the same cell overlap extensively and fasciculate in the mutant animals. Arbors of each cell project to the same general location as in wild type, but there are significant gaps in territory coverage.

Individual ddaD neurons of Dscam23/Dscam47 larvae show significant dendrite crossing, indicating defects in self-avoidance.

Single cell homozygous da neuron clones show defects in self-avoidance, with dendrites of the single cell overlapping extensively. These defects are seen in single cell clones of class I da neurons (such as ddaD), class II da neurons (such as ldaA), class III da neurons (such as ddaA) and class IV da neurons (such as ddaC). Targeting is grossly normal in these mutant clones, with two exceptions; in several clones, main dendritic trunks fail to properly segregate, leaving some regions of the body wall devoid of dendrites, and dendrites in the lateral regions of the body wall (from ldaB, ddaA and ldaA) form dense accumulations near the lateral chordotonal organ.

Class IV da neurons in Dscam21/Dscam23 larvae show self-avoidance defects, but the tiling pattern is not obviously disrupted compared to wild type.

Small clones of Dscam21 cells induced in the mushroom body at the early third instar and then examined 24-36 hours later are often seen as multiple fascicles (in contrast to wild-type control clones which form single fascicles). Defects in branching are also seen in the mushroom body lobes; the mutant clones still form two distinct branches, but often the branches fail to segregate dorsally and medially.

Or47a-expressing olfactory receptor neurons (ORNs) that are mutant for Dscam23 show marked mis-targeting of axons in the antennal lobe as they project towards wild-type targets (glomerulus DM3) on the ipsilateral side. The penetrance of the mistargeting phenotype is 100% with variable expressivity (on average about half of the mutant axons terminate in their correct glomerulus). P{GAL4}GH298-expressing ORNs that are mutant for Dscam23 often fail to project to their normal target (the V glomerulus). In about 50% of cases, mutant axons leave the nerve, turn ventrally as in wild type and innervate ectopic positions within the ventral region of the antennal lobe. In the remaining cases the mutant axons do not turn ventrally and terminate more dorsally, typically in more central and lateral regions of the lobe. Or22a-expressing and Or23a-expressing Dscam23 mutant ORNs target normally to the correct glomerulus. Or47b-expressing Dscam23 mutant ORNs show mistargeting to more dorsal regions of the antennal lobe than the normal target (the VA1 l/m glomerulus) and also targeting defects in the contralateral lobe. Or46a-expressing Dscam23 mutant ORNs frequently terminate upon entering the ventral central nervous system before reaching the antennal lobe, either immediately prior to entering the suboesophageal ganglion or upon exiting it, just ventral to the antennal lobe. The mutant ORNs form a structure with the appearance of a glomerulus where they terminate.

External Data
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Additional Comments
Genetic Interactions
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Xenogenetic Interactions
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Complementation and Rescue Data
Comments

The dendritogenesis defects (reduced number of dendritic tips) in the embryonic aCC motoneurons characteristic for Dscam123/Dscam121 transheterozygotes cannot be rescued by expression of Dscam1exon17.2.Scer\UAS.T:Avic\GFP under the control of Scer\GAL4eve.RN2 but is fully rescued when both Scer\GAL4eve.RN2 and Scer\GAL4GMR23E04 driver are used simultaneously - but only in the aCC that are associated with MP1 neurons expressing Dscam1exon17.2.Scer\UAS.T:Avic\GFP (Scer\GAL4GMR23E04 drives expression in a random half of all MP1 cells).

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Synonyms and Secondary IDs (7)
References (16)