FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\capsC28fs
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General Information
Symbol
Dmel\capsC28fs
Species
D. melanogaster
Name
FlyBase ID
FBal0241555
Feature type
allele
Associated gene
Dmel\caps
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Sakurai et al., 2007)
Progenitor genotype
Cytology
Description

Carries a frame-shift mutation at position C28 in the in the signal peptide region of the caps protein.

(Sakurai et al., 2007)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
sequence_alteration
3L:13,275,770..13,275,772 [+]
Comment:

Reported as a frameshift in the C28 residue.

(Sakurai et al., 2007)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      Large eye clones of capsC28fs mutants exhibit defects in the medulla and R8 axon guidance. However, there are no defects in R8 axon bundling nor undershooting of the M3 target layer. capsC28fs R8 axons extend over their target layer M3 and terminate at M4 or M5 at very low frequency. In contrast, capsC28fs mutant R7 axons do not show any targeting phenotype.

      Expression of capsScer\UAS.cSa in R7 and R8 photoreceptors, under the control of Scer\GAL4GMR.PF, in a transheterozygous capsC28fs/Df(3L)Exel6118 background display the same R7 mistargeting phenotype as found upon expression of capsScer\UAS.cSa in a wild-type background.

      (Berger-Müller et al., 2013)

      Lateral neuroblast clones in the antennal lobe that are homozygous for capsC28fs result in two types of dendrite targeting defects; loss of innervation in glomeruli that are normally targets of lateral projection neurons and gain of innervation in glomeruli that are normally not the targets of lateral projection neurons. All of the glomeruli that show loss of innervation are normally targets of caps-positive projection neurons, whereas the ectopically innervated glomeruli are mostly normally targets of caps-negative projection neurons.

      DL1, DA1, DC3 and VA1d projection neurons (all normally caps-negative) do not have any detectable dendrite targeting defects when made homozygous for capsC28fs using MARCM.

      VC1, VC2, VA4 and DM1 projection neurons (all normally caps-positive) that have been made homozygous for capsC28fs using MARCM show innervation of additional ectopic glomeruli that are normally targeted by caps-negative projection neurons. All homozygous VC1 projection neurons show strong ectopic innervation, and 92% of this ectopic innervation occurs in the DA2, DC2, VM7, DC1 and VM5 glomeruli. Loss of caps function in VC2, VA4 and DM1 projection neuron clones results in strong ectopic innervation of the VM7, DA2 and VM5 glomeruli.

      Nine classes of olfactory receptor neuron show no obvious axon-targeting defects in animals in which approximately half of all olfactory receptor neurons are homozygous for capsC28fs.

      DL1 projection neurons show normal dendrite targeting in adult escaper capsC28fs/Df(3L)Exel6118 animals.

      The dendrite targeting defects of single-cell DL1 projection neuron clones expressing capsScer\UAS.cSa under the control of Scer\GAL4GH146 are still seen in a capsC28fs/Df(3L)Exel6118 background.

      (Hong et al., 2009)

      Compared to wild-types, the number of contact points is reduced between myopodia and growth cones in capsC28fs/Df(3L)Ly mutant embryos. The number of free myopodia that do not contact the growth cone is unchanged in the mutants.

      There is a delay in the formation and reduction in size of presynaptic terminals on ventral muscle 12 in capsC28fs/Df(3L)Ly mutant embryos compared to wild-type controls.

      (Kohsaka and Nose, 2009)

      No defects are apparent in capsC28fs single mutant clones during leg segmentation. Similarly to wild-type clones, capsC28fs single mutant clones display irregular boundaries.

      With regards to capsC28fs mutant clones in the leg imaginal disc, the displacement rate of cells from tarsal segment 5 to to the pretarsal segment is reduced from the 95.2% in wild-type clones to 68.8% in the mutants.

      (Sakurai et al., 2007)
      External Data
      Interactions
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      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Lateral neuroblast clones in the antennal lobe that are doubly homozygous for capsC28fs and Df(3L)trnΔ17 show two types of dendrite targeting defects; loss of innervation in glomeruli that are normally targets of lateral projection neurons and gain of innervation in glomeruli that are normally not the targets of lateral projection neurons. Loss of innervation of the VA7m, VC1 and VC2 glomeruli is frequently seen in the double mutant embryos.

      (Hong et al., 2009)

      Compared to the respective single mutants, the number of contact points is further reduced between myopodia and growth cones and length of axon terminals is much shorter in capsC28fs, Df(3L)trnΔ17 double mutant embryos. Some muscles are completely lacking synaptic terminals in the double mutants.

      (Kohsaka and Nose, 2009)

      The distal to proximal progression of the presumptive tarsal segment 5/pretarsus boundary is delayed in some Df(3L)trnΔ17, capsC28fs clones during leg segmentation.

      Df(3L)trnΔ17, capsC28fs clones generated by the minute technique cause stunted pretarsal segments and claws in addition to defective joint formation at the tarsal segment 4/tarsal segment 5 and tarsal segment 5/pretarsus boundaries in the adult leg.

      Compared to single mutant or wild-type controls, Df(3L)trnΔ17, capsC28fs double mutant clones are more rounded in shape and have smoother boundaries.

      The displacement rate of cells from tarsal segment 5 to to the pretarsal segment is further reduced from the 68.8%% in capsC28fs single mutant clones to 26.7% in Df(3L)trnΔ17, capsC28fs double mutants.

      (Sakurai et al., 2007)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      capsC28fs is rescued by capsUAS.cSa/Scer\GAL4GH146

      (Hong et al., 2009)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      C28fs
      (Sakurai et al., 2007)
      capsC28fs
      (Roy et al., 2014, Kohsaka and Nose, 2009, Sakurai et al., 2007)
      capsc28fs
      (Berger-Müller et al., 2013, Hong et al., 2009, Hong et al., 2009)
      Name Synonyms
      Secondary FlyBase IDs
        References (6)