FB2025_01 , released February 20, 2025
Allele: Dmel\MiroSd32
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General Information
Symbol
Dmel\MiroSd32
Species
D. melanogaster
Name
FlyBase ID
FBal0240382
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DMirosd32
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description

A 29 bp deletion and frame-shifts Miro at Y89, adding 12 abnormal amino acids before terminating.

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 ( 1 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In

bouton & neuromuscular junction | larval stage (with MiroB682)

mitochondrion & motor neuron | larval stage (with MiroB682)

mitochondrion & neuron | larval stage (with MiroB682)

Detailed Description
Statement
Reference

Homozygous ventral midline precursor cells do not divide more often than wild-type precursors.

Heterozygous MiroSd32 mutants display mitochondrial mislocalisation in neurons.

In the motor neurons of MiroB682/MiroSd32 larvae, mitochondria are largely absent from neuro-muscular junctions, and are present in reduced numbers in axons, mainly concentrated close to the ventral ganglion. The proportion of motile mitochondria is significantly reduced in these cells and, unlike in wild-type, many stationary mitochondria are not clustered. In addition, the motile mitochondria (both anterograde and retrograde) are significantly smaller than in wild-type.

Gross eye morphology is normal but phototaxis is defective in flies whose eyes are homozygous for MiroSd32.

In neurons of MiroSd32/MiroB682 larvae, mitochondria are retained in the cell bodies and not properly distributed to neuronal processes - most neuromuscular junctions lack mitochondria.

Bouton morphology and distribution is abnormal at neuromuscular junctions in MiroB682/MiroSd32 larvae.

In MiroSd32/MiroB682 larvae, excitatory junction potential evoked by 10Hz stimulation of neuro-muscular junctions (NMJs) starts off normal, but, unlike wild-type, rapidly decays.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Phenotype Manifest In
NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference

MiroSd32 heterozygosity enhances the locomotor defects in flies induced by Scer\GAL4elav-C155-driven overexpression of Hsap\APPAβ1-42.Scer\UAS.cIa.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
Reported As
Name Synonyms
Secondary FlyBase IDs
  • FBal0239857
  • FBal0239813
References (10)