A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\MiroSd32

General Information
SymbolDmel\MiroSd32SpeciesD. melanogaster
NameFlyBase IDFBal0240382
Feature typealleleAssociated geneDmel\Miro
Also Known AsMirosd32
Allele classloss of function allele
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
A 29 bp deletion and frame-shifts Miro at Y89, adding 12 abnormal amino acids before terminating.
Cytology
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bouton & neuromuscular junction | larval stage (with MiroB682)
mitochondrion & motor neuron | larval stage (with MiroB682)
mitochondrion & neuron | larval stage (with MiroB682)
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Statement
Reference
Homozygous ventral midline precursor cells do not divide more often than wild-type precursors.
Heterozygous Miro[Sd32] mutants display mitochondrial mislocalisation in neurons.
In the motor neurons of Miro[B682]/Miro[Sd32] 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 Miro[Sd32]. In neurons of Miro[Sd32]/Miro[B682] 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 Miro[B682]/Miro[Sd32] larvae. In Miro[Sd32]/Miro[B682] larvae, excitatory junction potential evoked by 10Hz stimulation of neuro-muscular junctions (NMJs) starts off normal, but, unlike wild-type, rapidly decays.
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Statement
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Statement
Reference
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Statement
Reference
Miro[Sd32] heterozygosity enhances the locomotor defects in flies induced by Scer\GAL4[elav-C155]-driven overexpression of Hsap\APP[Aβ1-42.Scer\UAS.cIa].
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Fails to complement
Partially rescued by
Comments
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hide Synonyms & Secondary IDs ( 5 )
Reported As
Symbol Synonym
MiroSd32
 
Mirosd32
Name Synonym
Secondary FlyBase IDs
  • FBal0239813
  • FBal0239857
hide References ( 6 )
Research paper
Bossing et al., 2012, Dev. Cell 23(2): 433--440
Disruption of Microtubule Integrity Initiates Mitosis during CNS Repair. [FBrf0219196]
Iijima-Ando et al., 2009, PLoS ONE 4(12): e8310
Mitochondrial mislocalization underlies Abeta42-induced neuronal dysfunction in a Drosophila model of Alzheimer's disease. [FBrf0209556]
Russo et al., 2009, J. Neurosci. 29(17): 5443--5455
Drosophila Miro is required for both anterograde and retrograde axonal mitochondrial transport. [FBrf0207789]
Mast et al., 2008, Development 135(15): 2669--2679
Reactive oxygen species act remotely to cause synapse loss in a Drosophila model of developmental mitochondrial encephalopathy. [FBrf0207179]
Guo et al., 2005, Neuron 47(3): 379--393
The GTPase dMiro is required for axonal transport of mitochondria to Drosophila synapses. [FBrf0188178]
FlyBase analysis
FlyBase, 1992-, FlyBase curation.
FlyBase curation. [FBrf0105495]