A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\MiroB682

General Information
SymbolDmel\MiroB682SpeciesD. melanogaster
NameFlyBase IDFBal0239855
Feature typealleleAssociated geneDmel\Miro
Also Known AsdMiroB682
Map ( GBrowse ) GBrowse View Helpdetailed view FBal0239855 FBal0239858
Allele classloss of function allele
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
point mutation
na_change=G19862960A
reported_na_change=G?A
pr_change=W104 | Miro-PD; W104 | Miro-PE; W104 | Miro-PC; W104 | Miro-PF
reported_pr_change=W105@
comment=Reported as a W105 to UAG nonsense mutation.
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Amino acid replacement: W105@.
Cytology
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bouton & neuromuscular junction | larval stage
bouton & neuromuscular junction | larval stage (with MiroSd32)
microtubule & bouton
mitochondrion & motor neuron | larval stage (with MiroSd32)
mitochondrion & neuron | larval stage
mitochondrion & neuron | larval stage (with MiroSd23)
mitochondrion & neuron | larval stage (with MiroSd26)
mitochondrion & neuron | larval stage (with MiroSd32)
mitochondrion & somatic muscle | larval stage
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Statement
Reference
In Miro[B682] mutants the majority of mitochondria remain stranded in the neuronal soma and soma-proximal axon, whereas the distal axon and presynaptic nerve terminal are largely devoid of mitochondria. There is no evidence of NMJ degeneration or altered neuromuscular growth.
Stimulus-dependent or resting cytosolic Ca[2+] levels are not affected by the chronic lack of mitochondria in motor neuron-terminals of Miro[B682] mutants.
Mutant neuromuscular junctions show reliable homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.
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 shorter than in wild-type. There is also a small but significant reduction in the proportion of mitochondria that are motile and in the rate of mitochondrial flux in the axons of in motor neurons of Miro[B682]/+ larvae.
Gross eye morphology is normal but phototaxis is defective in flies whose eyes are homozygous for Miro[B682]. Homozygous Miro[B682] larvae are small and have reduced muscles. They tend to wiggle on the spot, rather than moving forwards. Anterior segments show rhythmic contractions, but posterior segments are sluggish, sometimes paralyzed. In neurons of Miro[B682]/Miro[B682], Miro[Sd23]/Miro[B682], Miro[Sd26]/Miro[B682] or Miro[Sd32]/Miro[B682] larvae, mitochondria are retained in the cell bodies and not properly distributed to neuronal processes - most neuromuscular junctions lack mitochondria. The somatic muscles of Miro[B682]/Miro[B682] larvae also show highly abnormal distribution of mitochondria. However, the mitochondria in these animals show no structural abnormalities and have normal membrane potentials. In contrast to the effect on mitochondria, vesicle transport in the neurons of these animals is only weakly abnormal. Bouton morphology and distribution is abnormal at neuromuscular junction in Miro[B682]/Miro[B682] and Miro[B682]/Miro[Sd32] larvae. The arrangement of microtubules in the boutons of Miro[B682]/Miro[B682] larvae is also abnormal, but the actin cytoskeleton in these boutons appears normal. In Miro[B682]/Miro[B682] larvae, resting Ca2+ concentration at neuro-muscular junctions is higher than normal. 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. This phenotype is also seen in Miro[B682]/Miro[B682], Miro[B682]/Df(3R)mbc-R1 or Miro[B682]/Miro[Sd26] larvae, but not in Miro[B682]/Miro[Sd23] larvae. Prolonged 10Hz stimulation also leads to greater increases in Ca2+ concentration at NMJs than in wild-type. Miro[B682]/Miro[B682] also show a significant increase in spontaneous mini excitatory junction potentials following 10Hz stimulation of neuro-muscular junctions.
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Statement
Reference
Homozygous Miro[B682] suppresses the neuromuscular degeneration seen when α-Spec[KK101541] is expressed under the control of Scer\GAL4[elav-C155]. The decrease in the number of mitochondria seen in Miro[B682] mutants is also seen in these larvae.
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Statement
Reference
hide Complementation & Rescue Data
Fails to complement
Partially rescued by
Not rescued by
Comments
Miro[Scer\UAS.cGa]; Scer\GAL4[elav-C155] rescues most of the phenotypes due to Miro[B682]/Miro[B682]: larval lethality, larval body and muscle size, distribution of mitochondria to the distal extremities of neurons, neuro-muscular junction morphology and microtubule cytoskeleton organization. None of these phenotypes are rescued by Miro[Scer\UAS.cGa]; Scer\GAL4[how-24B].
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hide Synonyms & Secondary IDs ( 4 )
Reported As
Symbol Synonym
MiroB682
 
Name Synonym
Secondary FlyBase IDs
hide References ( 5 )
Research paper
Keller et al., 2011, Neuron 72(5): 760--775
Glial-derived prodegenerative signaling in the Drosophila neuromuscular system. [FBrf0216904]
Chouhan et al., 2010, J. Neurosci. 30(5): 1869--1881
Presynaptic mitochondria in functionally different motor neurons exhibit similar affinities for Ca2+ but exert little influence as Ca2+ buffers at nerve firing rates in situ. [FBrf0209911]
Dickman and Davis, 2009, Science 326(5956): 1127--1130
The schizophrenia susceptibility gene dysbindin controls synaptic homeostasis. [FBrf0209454]
Russo et al., 2009, J. Neurosci. 29(17): 5443--5455
Drosophila Miro is required for both anterograde and retrograde axonal mitochondrial transport. [FBrf0207789]
Guo et al., 2005, Neuron 47(3): 379--393
The GTPase dMiro is required for axonal transport of mitochondria to Drosophila synapses. [FBrf0188178]