FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\mys10
Open Close
General Information
Symbol
Dmel\mys10
Species
D. melanogaster
Name
FlyBase ID
FBal0012687
Feature type
allele
Associated gene
Dmel\mys
Associated Insertion(s)
Carried in Construct
Also Known As
mysXB87, l(1)mysXB87
Key Links
Genomic Maps

Allele class

loss of function allele

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Bunch et al., 1992)

loss of function allele

(Jannuzi et al., 2002, Volk et al., 1990, Zusman et al., 1990)
Mutagen
ethyl methanesulfonate
(Zusman et al., 1990)
Progenitor genotype
Cytology
Description

Nucleotide substitution: G?A. Mutation at exon 3 splice acceptor site.

(Jannuzi et al., 2002)

Indistinguishable from wild type on Southern blot. Faint residual band on immunoblots (as for Df(1)C128) where product is thought to be a remnant from the maternal supply.

(Bunch et al., 1992)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:8,064,532..8,064,532 [+]
Nucleotide change:

G8064532A

Comment:

Reported as a G to A mutation in the splice acceptor. No protein detected in mutants.

(Jannuzi et al., 2002)
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

      Stage 14 oocytes carrying mys10 somatic clones are much more rounded than wild-type.

      (Bateman et al., 2001)

      Homozygous clones in the wing produce discrete, round blisters of variable size. These blisters can be located anywhere on the wing. Wing venation is normal.

      (Prout et al., 1997)

      Clones present in the wing 4-6 hours after pupariation (AP) cause no morphological abnormalities. In 30 and 36 hour AP dorsal and ventral clones are associated with pronounced matrix-filled blisters. Blisters result from failure of mutant clone cells to reappose with normal cells in the opposite surface. Both mutant and normal cells generally fail to undergo the cell shape changes required for re-apposition. Clones induced late in larval development may be long but only a few cells wide, the dorsal and ventral surfaces in the adult wing are separated.

      (Brabant et al., 1996)

      Dorsal wing clones as small as 50 cells display a wing blister phenotype.

      (Brower et al., 1995)

      No anti-βPS staining at muscle attachment sites.

      (Bunch et al., 1992)

      Cells derived from homozygous late gastrula embryos appear less stretched out and more rounded and have fewer cell-cell contacts than wild-type cells when cultured in vitro on laminin-coated coverslips.

      (Volk et al., 1990)

      Folds in one or both surfaces of the wing, wing blisters, vein abnormalities and missing or enlarged halteres were seen in adults mosaic for mys function.

      (Zusman et al., 1990)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhancer of
      Statement
      Reference

      mys10/mys[+] is an enhancer of visible | dominant phenotype of sogEP7

      (Araujo et al., 2003)

      mys10/mys[+] is an enhancer of visible | dominant phenotype of sogEP11

      (Araujo et al., 2003)
      Phenotype Manifest In
      Enhancer of
      Statement
      Reference

      mys10/mys[+] is an enhancer of wing vein phenotype of sogEP7

      (Araujo et al., 2003)

      mys10/mys[+] is an enhancer of wing vein phenotype of sogEP11

      (Araujo et al., 2003)

      mys10/mys[+] is an enhancer of oocyte phenotype of Lar5.5/Lar13.2

      (Bateman et al., 2001)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Small mys10 somatic clones in the wing generated a sogEP7 background cause distinct vein phenotypes: Dorsal clones that cross over or lie adjacent to longitudinal veins, such as L4 and L5 induce the formation of veins with diffuse borders that are less compact, less pigmented and wider than normal veins. Dorsal clones running over L3 induce dramatic vein thickening and diffuse vein borders. In contrast, ventral clones have no effect on veins.

      (Araujo et al., 2003)

      When tested in the odour-induced jump test, mutants with the heteroallelic combination of mys10 with swsolfE-x26 show normal responses to iso-amyl acetate, ethyl acetate and benzaldehyde compared to controls.

      (Ayyub and Paranjape, 2002)

      mys10 ifB4 double mutant embryos show dorsal herniation.

      (Jannuzi et al., 2002)

      The addition of mys10/+ to Lar5.5/Lar13.2 increases the penetrance of the oocyte elongation phenotype from 14.1% to 48.7%.

      (Bateman et al., 2001)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Maternal germline clonal analysis demonstrates a maternal effect lethal phenotype that is rescuable by introduction of the wild-type copy of the gene from the father.

      (Perrimon et al., 1989)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      References (14)