FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\caps65.2
Open Close
General Information
Symbol
Dmel\caps65.2
Species
D. melanogaster
Name
FlyBase ID
FBal0091535
Feature type
allele
Associated gene
Dmel\caps
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
P-element activity
(Shishido et al., 1998)
Progenitor genotype
capsE2-3-27
(Shishido et al., 1998)
Cytology
Description

Deletion of exon 1 of caps, including P{lacW} of the progenitor capsE2-3-27.

(Shishido et al., 1998)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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

      caps65.2 homozygotes have a low penetrance of ISNb targeting defects.

      (Kurusu et al., 2008)

      caps65.2 embryos show discontinuous dorsal trunk formation, which is more severe at stage 14 (20.4% interruptions vs 0.2% in wild-type embryos) than at later stages (12.4% vs 0.4% in wild type). The amount of lateral trunk breaks are not significantly decreased in caps65.2 embryos compared to wild type.

      (Krause et al., 2006)

      Photoreceptor cell axon projection patterns appear normal in early pupae, while at the mid-pupal stage, gaps are seen in the R8 terminal layers of the medulla. Photoreceptor cell axon targeting in the medulla is highly disorganised in homozygous adult flies. The regular array of fascicles is disrupted and many axons cross over neighbouring bundles and/or terminate in abnormal positions.

      (Shinza-Kameda et al., 2006)

      Somatic clones in the wing disc homozygous for caps65.2 have shapes indistinguishable from wild-type control clones.

      (Milan et al., 2002)

      62% of homozygous embryos fail to hatch, though all those that do hatch develop into normal looking larvae. Very few (3%) survive to adulthood. In homozygous mutant embryos, the SNb enters the ventral muscle field and the RP neurons defasciculate normally. Furthermore, RP1, RP3 and RP4 properly synapse with their respective target muscles, whereas the RP5 axons stall, show enlarged growth cone like structures and fail to contact the target muscle. Instead the RP5 axons are split and found also in direct contact with the transversal nerve.

      (Abrell and Jackle, 2001)

      Homozygous clones do not cause observable alterations in the wing disc.

      (Milan et al., 2001)

      Most of the mutants die late in embryogenesis or soon after hatching, although a few survive to adulthood. No gross abnormalities occur in the CNS or musculature, but the target specificity of muscle 12 motorneurons is altered. The terminal branch of the ISNb is accompanied by additional varicosities on muscle 13, thus the restriction to muscle 12 is lost.

      (Shishido et al., 1998)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      Enhancer of
      Statement
      Reference

      caps65.2/caps[+] is an enhancer of visible | dominant phenotype of Bx1

      (Bejarano et al., 2008)

      caps65.2/caps65.2 is an enhancer of abnormal neuroanatomy | recessive phenotype of trnS064117

      (Kurusu et al., 2008)

      trnΔ2.9/caps65.2 is an enhancer of visible phenotype of Bx1

      (Milan et al., 2001)
      Other
      Statement
      Reference

      Chie5.5, caps65.2, trnΔ2.9 has visible phenotype

      (Milan et al., 2001)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      trn28.4, caps65.2 double mutant embryos show an additive phenotype, where the sum of the gaps in the dorsal and lateral trunks seen in single mutants is close to the figure seen in the double mutants.

      (Krause et al., 2006)

      Laterally located somatic clones in the wing disc that are homozygous for both trnΔ2.9 and caps65.2 have smoother borders than wild-type control clones. This phenotype is not see in medially located clones.

      (Milan et al., 2002)

      Kr1, KrmCD, caps05121 double homozygotes develop strong SNb phenotype; the SNb is absent in most of the double mutants analysed or do not extend beyond its second choice point close to muscle 28. In only a few cases the SNb stalls in the ventral muscle field.

      (Abrell and Jackle, 2001)

      caps65.2 trnΔ2.9 double mutant clones in the wing disc do not cause defects at the dorsal/ventral boundary but do perturb medial-lateral cell interactions.

      (Milan et al., 2001)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (1)
      Reported As
      Symbol Synonym
      caps65.2
      (Roy et al., 2014, Kohsaka and Nose, 2009, Bejarano et al., 2008, Kurusu et al., 2008, Krause et al., 2006, Shinza-Kameda et al., 2006)
      Name Synonyms
      Secondary FlyBase IDs
        References (10)