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General Information
Symbol
Dmel\sizU112
Species
D. melanogaster
Name
FlyBase ID
FBal0095211
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
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
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

Homozygous stage 16 embryos show a strong defect in myoblast fusion.

sizC1-28/sizU112 embryos show a strong defect in myoblast fusion.

The number of commissural fibers crossing the ventral midline of stage 16 embryos is reduced in sizU112 homozygotes and sizU112/sizC1-28 animals. This effect is seen most strongly in abdominal segments A1-A4. The longitudinal connectives are also thinner. In neuromeres with reduced commissures the midline glial cells migrate toward the connectives. The commissural phenotypes of these embryos are stronger than those of sizC1-28 homozygotes. In stage 16 sizU112/sizC1-28 embryos many axons that usually cross the ventral midline fail to do so and show fasciculation defects.

Mutants show a variable reduction in the number of commissural fibers. Midline glial cell is initially normal but reduced later due to loss of commissural axons.

3-5 neuromeres lack one or both commissures in homozygous embryos.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

The defects in myoblast fusion seen in sizC1-28/sizU112 embryos are partially suppressed by CadNM19 and multinucleate muscles are formed.

Reduction of ventral nerve cord commissures in stage 16 sizU112 homozygous embryos is strongly enhanced by Df(1)RK2, and by fra23H9. NetBScer\UAS.cHa; Scer\GAL4sim.PS largely suppresses the reduction of ventral midline commissures in sizU112 embryos. Reduction of ventral commissures in these embryos is also dominantly suppressed by sli550 and roboO1-103.

sizU112 fraC1-62 double mutant embryos lack most commissural axons.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Reduction of ventral nerve cord commissures in sizU112 homozygotes is rescued by sizP1.Scer\UAS or sizP2.Scer\UAS with Scer\GAL4sim.PS or Scer\GAL4sli.PS.

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Mutant
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Stocks (0)
Notes on Origin
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (4)