FB2024_03 , released June 25, 2024
Allele: Dmel\OliΔ9
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General Information
Symbol
Dmel\OliΔ9
Species
D. melanogaster
Name
FlyBase ID
FBal0284100
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Imprecise excision of the progenitor insertion resulting in a 1.53kb deletion extending from 802bp upstream to 732bp downstream of the Oli translation start site.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

Reported as a 1.53 kb deletion resulting from the imprecise excision of P{GSV2}OliGS5080, which extends from 802 bp upstream to 732 bp downstream of the Oli translation start.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

Approximately 80.4% of homozygous embryos survive to the larval stage. Under non-crowded conditions, only 42% of adults emerge from the pupal case. Under normal population conditions, only 3.4% of homozygotes emerge as adults.

Homozygous wandering stage third instar larvae remain largely on the surface on agar plates, in contrast to wild-type larvae which burrow into the agar at this stage. The mutant larvae show irregular, slower crawling behaviour compared to wild type and frequently appear to drag their abdominal segments. Homozygous adult escapers are unable to fly and have slow, uncoordinated leg movements, circling and wobbling.

The distribution and number of ventral nerve cord glia and the organisation of the ventral nerve cord scaffold appear normal in mutant embryos. The number and positions of eve-positive neurons also appear normal.

Btau\MAPTisl.H.T:Hsap\MYC-positive motorneuron axons show abnormal trajectories at the ventral nerve cord exit in mutant embryos; they fail to exit via the transverse nerve (TN) in 54.6% of hemisegments and ectopically extend axons through the SN branch in 58.8% of hemisegments. ISNb and TN motorneurons show muscle targeting defects in 51.7% of hemisegments. In 19.3% of hemisegments, ISNb motorneuron axons do not correctly defasciculate from each other, resulting in the stalling of thicker axon bundles between muscles 6 and 13 and a failure to innervate the muscle 12/13 cleft. In 27.8% of hemisegments, ISNb or TN axons extend processes that form abnormal contacts between them and in 14.2% of hemisegments, lateral bipolar dendrite /TN neurons have ectopic processes onto ventral muscles.

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

The penetrance of the phenotype seen in both OliΔ9 (19.3%) and exexKK30/exexGal4 (34.4%) single mutant embryos where ISNb motorneuron axons do not correctly defasciculate from each other and fail to innervate the muscle 12/13 cleft is increased in double mutants to 68.5%.

Xenogenetic Interactions
Statement
Reference

Expression of Ggal\Olig2Scer\UAS.cOa under the control of Scer\GAL4elav-C155 partially rescues eclosion rates and walking defects in OliΔ9 adults.

Complementation and Rescue Data
Not rescued by
Comments

Expression of OliScer\UAS.cOa under the control of Scer\GAL4elav-C155 fails to rescue the motorneuron axon targeting defects seen in OliΔ9 embryos. Survival to adulthood and adult locomotor defects are significantly rescued.

Expression of OliScer\UAS.cOa under the control of Scer\GAL4sca.PU partially rescues the motorneuron axon targeting defects seen in OliΔ9 embryos. Survival to adulthood and adult locomotor defects are significantly rescued.

Expression of OliScer\UAS.cOa under the control of Scer\GAL4repo fails to rescue eclosion rates or walking defects in OliΔ9 adults.

Expression of OliScer\UAS.cOa under the control of Scer\GAL4VGlut-OK371 partially rescues eclosion rates and walking defects in OliΔ9 adults.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (2)