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General Information
Symbol
Dmel\Dr72
Species
D. melanogaster
Name
FlyBase ID
FBal0086878
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

Point mutant.

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

Dr72/Df(3L)fz-GS1a animals show strong embryonic CNS defects. These are made worse when DΔHMG.Scer\UAS or DScer\UAS.T:Rep-en are expressed via Scer\GAL4sim.P3.7 in this background.

No loss of CQ neurons is seen in Dr72 embryos. 3% of hemisegments show loss of RP2 neurons, while duplication of RP2 is seen in 8% of hemisegments. Expansion of the eve lateral cluster (ELC) is seen in 1% of hemisegments. 16% of hemisegments show duplication of cells at the position of the aCC/pCC neurons. Neuroblast NB5-3 is missing in 2% of hemisegments.

Shows null embryonic segmentation defect.

80% of hemizygous embryos have severe defects throughout the nerve cord, showing thinning of longitudinal connectives and fusion of commissures. The number of midline glia cells per segment is reduced compared to wild-type embryos. The remaining midline glia cells are more frequently located anterior to the anterior commissure than in wild-type embryos. The cell bodies of the midline glia lie along the ventral surface of the commissures and do not migrate and ensheath the commissures. The axonal defects of Dr72/Df(3L)fz-GS1a embryos are rescued in the majority of cases if the embryos are expressing DScer\UAS.cSa under the control of Scer\GAL4sim.PS. The number and location of the midline glia cells is also rescued.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Suppressed by
Enhancer of
Statement
Reference

Dr72/D[+] is an enhancer of denticle phenotype of SoxNU6-35

Dr72 is an enhancer of neuroblast NB5-3 phenotype of SoxNU6-35

Other
Additional Comments
Genetic Interactions
Statement
Reference

Dr72/+ strongly enhances the loss of denticle phenotype seen in SoxNU6-35 embryos, such that denticle formation is almost completely abolished.

Dr72 SoxNU6-35 double mutant embryos show severe disruption in the organisation and structure of the central nervous system. There is a complete loss of longitudinal axons in many segments and frequent gaps in the neuropil. Commissures are often absent, and those that do form are virtually never separated. The aCC/pCC and CQ neurons are missing in at least 15% of hemisegments. RP2 neurons are missing in 94% of hemisegments and eve lateral cluster neurons are missing in 99% of hemisegments. Neuroblast NB5-3 is missing in 79% of hemisegments.

Xenogenetic Interactions
Statement
Reference

Scer\GAL4sim.P3.7-mediated expression of Mmus\Sox2Scer\UAS.T:Avic\GFP-EYFP suppresses, whereas expression of Mmus\Sox2ΔHMG.Scer\UAS.T:Avic\GFP-EYFP,T:Hsap\MYC or Mmus\Sox2Scer\UAS.T:Rep-en,T:Hsap\MYC enhances the embryonic CNS defects of Dr72/Df(3L)fz-GS1a animals.

The axonal defects seen in Dr72/Df(3L)fz-GS1a embryos are rescued in many cases if the embryos are expressing Mmus\Sox2Scer\UAS.cSa under the control of Scer\GAL4sim.PS.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (8)