FB2024_03 , released June 25, 2024
Allele: Dmel\mir-8Δ
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General Information
Symbol
Dmel\mir-8Δ
Species
D. melanogaster
Name
FlyBase ID
FBal0297315
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Cytology
Description

FLP-mediated recombination between the two progenitor insertions P{XP}d01682 and PBac{WH}f05125 has deleted the sequence between them, removing the mir-8 miRNA.

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

Homozygous larvae show a decrease in the number of type 1b synaptic boutons and the number of axonal branches at the neuromuscular junction compared to controls at the second and third instar stages. There is a significant reduction in subsynaptic reticulum thickness, area and fold complexity compared to controls, while presynaptic bouton area is normal.

In both wild type and mir-8Δ/mir-8Δ embryos, the intersegmental nerve branch ISNb motor axons show normal trajectories to reach ventral muscle targets; subsequent to target recognition, mir-8Δ/mir-8Δ embryos show an innervation defect (innervation of the cleft between m6 and m7 is undetectable or reduced). mir-8Δ/+ embryos show an ISNb defect at an intermediate frequency. mir-8Δ/mir-8Δ embryos show significant decreases in synaptic contact at m6/m7, compared to controls. RP3 axon terminals in 15h old mutant embryos show abnormalities: around 50% of RP3 motor axons show sprouting of filopodia significantly increases (with less well-defined elaboration of the neuromuscular junction between m6/m7), and RP3 axon terminals frequently extend to and form varicosities on neighboring non-target muscle (m13).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
NOT suppressed by
Statement
Reference

mir-8Δ has axon | embryonic stage phenotype, non-suppressible by ena23/ena[+]

mir-8Δ has axon | embryonic stage phenotype, non-suppressible by ena[+]/ena210

Other
Additional Comments
Genetic Interactions
Statement
Reference

mir-8Δ/+ ; cpbF44/+ double transheterozygous larvae show a decrease in the number of boutons and in presynaptic arbor expansion at the neuromuscular junction (normalised to muscle area) compared to controls.

ena23/+ or ena210/+ does not rescue the neuromuscular junction formation phenotype (intersegmental nerve branch ISNb motor axon innervation defects at m6/7) seen in mir-8Δ/+ embryos.

Expression of Nrg180.I.Scer\UAS driven by Scer\GAL4elav.PU significantly partially suppresses the intersegmental nerve branch ISNb motor axon innervation defects (at m6/7) seen in mir-8Δ/mir-8Δ embryos. Expression of Nrg180.I.Scer\UAS driven by Scer\GAL4how-24B significantly partially (only 10%) suppresses the intersegmental nerve branch ISNb motor axon innervation defects (of m6/7) seen in mir-8Δ/mir-8Δ embryos.

Xenogenetic Interactions
Statement
Reference

Expression of Zzzz\actAFP4mito.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4how-24B rescues the reduction in subsynaptic reticulum area seen at the neuromuscular junction in homozygous mir-8Δ larvae.

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 (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (2)