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General Information
Symbol
Dmel\Drp12
Species
D. melanogaster
Name
FlyBase ID
FBal0176234
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    Mutation identified by sequence analysis.

    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 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference

    Drp12 homozygous mutant MARCM clones of glutamatergic neurons in the proximal wing have significantly increased mitochondrial length in the axons and mitochondrial hyperfusion in the cell bodies, compared to controls.

    Drp11/Drp12 transheterozygote mutants are lethal.

    Drp12 mutant retinal clones do not exhibit lipid droplet accumulation. Aconitase activity is reduced in these mutants and there is a strong correlation between decreased aconitase enzymatic activity and the number of lipid droplets per ommatidium, suggesting reactive oxygen species may play a role in lipid droplet accumulation.

    The electroretinogram has a normal amplitude but shows loss of the on- and off-transients in mutant adults.

    Drp11/Drp12 flies do not show clumping of mitochondria or muscle cell death in the indirect flight muscles.

    In Drp11/Drp12 mutant adult flight muscles, the mitochondria are enlarged (being round in shape) and fewer in number compared to wild type but contain intact internal structures.

    Drp11/Drp12 cells contain fewer mitochondria per cell than wild type and mitochondrial morphology is abnormal.

    Stimulus-dependent or resting cytosolic Ca[2+] levels are not affected by the chronic reduction of mitochondria in motor neuron-terminals of Drp12 mutants.

    Shows defects in neurotransmitter release.

    Homozygous third larval instar salivary gland cells show clustering of mitochondria.

    Homozygous third larval instar brains show reduced levels of mitochondria in the neuropil and clumps of mitochondria in the motor neuron cell bodies bordering the ventral nerve cord.

    Fewer mitochondria than normal are seen in the axons of homozygous motor neurons and they form long threads that are rarely seen in controls.

    Mitochondrial number per bouton is reduced at homozygous and Drp11/Drp12 neuromuscular junctions.

    Bouton number per muscle are and synapse length per muscle area are not different from those of controls in Drp12 neuromuscular junctions, although neuromuscular junction branching is slightly increased.

    Intracellular resting Ca[2+] in Drp12 boutons is approximately 2-fold higher than the level in controls.

    Neurotransmission at the neuromuscular junction (measured by the excitatory junctional potential (EJP) amplitude) is not affected when stimulated at 1Hz in 0.6mM, 1mM or 5mM extracellular Ca[2+] at 22[o]C, or in 5mM Ca[2+] at 36[o]C, and is only elevated in 0.25mM extracellular Ca[2+] in Drp12 mutants. At 0.25mM extracellular Ca[2+], controls fail to evoke EJPs in 20% of the stimulations, whereas Drp12 animals only fail 4% of the time.

    Drp12 mutants cannot maintain normal neurotransmission (measured by the EJP) during high frequency (10Hz) stimulation at 22[o]C in contrast to controls. This phenotype is exacerbated at 36[o]C and can be partially rescued by ATP.

    Endocytosis and exocytosis of endo cycling pool vesicles at the neuromuscular junction is not disrupted in stimulated Drp12 mutants, but the mutants show a defect in the cycling of reserve pool vesicles.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Suppressed by
    Statement
    Reference
    NOT suppressed by
    Statement
    Reference
    NOT Suppressor of
    Statement
    Reference

    Drp12/Drp1[+] is a non-suppressor of flightless phenotype of park1

    Drp12/Drp1[+] is a non-suppressor of visible phenotype of park1

    Drp12/Drp1[+] is a non-suppressor of visible phenotype of Pink1B9

    Drp12/Drp1[+] is a non-suppressor of flightless phenotype of Pink1B9

    Other
    Phenotype Manifest In
    Suppressed by
    NOT suppressed by
    Statement
    Reference
    Suppressor of
    Statement
    Reference
    NOT Suppressor of
    Statement
    Reference

    Drp12/Drp1[+] is a non-suppressor of wing phenotype of park1

    Drp12/Drp1[+] is a non-suppressor of adult thorax phenotype of park1

    Drp12/Drp1[+] is a non-suppressor of wing phenotype of Pink1B9

    Drp12/Drp1[+] is a non-suppressor of adult thorax phenotype of Pink1B9

    Drp12/Drp1[+] is a non-suppressor of mitochondrion & dopaminergic neuron phenotype of Pink1B9

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    The reduced connectivity of the mitochondrial network in body wall muscles characteristic for third instar larvae expressing maskHMS01045 under the control of Scer\GAL4how-24B cannot is not changed by combination with Drp11/Drp12.

    Drp12 suppresses the increase in the number of neuroblasts per clone seen in clones expressing Nint.U.Scer\UAS under the control of Scer\GAL4Act5C.PU.

    Expression of either MarfmiRNA.CDS.Scer\UAS, MarfmiRNA.UTR.Scer\UAS or opa1-likemiRNA.CDS.Scer\UAS under the control of Scer\GAL4elav.PU is sufficient to restore a normal filamentous mitochondrial network in Drp11/Drp12 flies.

    Expression of PmiScer\UAS.cRa under the control of Scer\GAL4elav.PU does not rescue mitochondrial morphology in Drp11/Drp12 flies.

    Flies expressing porinScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4Mef2.PR in a Drp12/+ background show defects in mitochondrial morphology in the indirect flight muscles, with smaller or almost completely abolished mitochondria.

    The downturned wing, crushed thorax and flightless phenotypes of Pink1B9 mutant flies are not suppressed by Drp12/+.

    The swollen mitochondria phenotype seen in dopaminergic neurons of Pink1B9 mutants is not suppressed by Drp12/+.

    Xenogenetic Interactions
    Statement
    Reference

    The lethality of Drp11/Drp12 transheterozygotes is rescued by expression of Hsap\DNM1LScer\UAS.cCa under the control of Scer\GAL4da.PU in the mutant background.

    The lethality of Drp11/Drp12 transheterozygotes is not rescued by expression of Hsap\DNM1LA395D.Scer\UAS under the control of Scer\GAL4da.PU in the mutant background.

    The lethality of Drp11/Drp12 transheterozygotes is not rescued by expression of Hsap\DNM1LG350R.Scer\UAS under the control of Scer\GAL4da.PU in the mutant background.

    The lethality of Drp11/Drp12 transheterozygotes is rescued by expression of Hsap\DNM1LE379K.Scer\UAS under the control of Scer\GAL4da.PU in the mutant background.

    Complementation and Rescue Data
    Comments

    The lethality of Drp11/Drp12 transheterozygotes is rescued by expression of Drp1Scer\UAS.cUa under the control of Scer\GAL4da.PU in the mutant background.

    Expression of Drp1Scer\UAS.cDa under the control of Scer\GAL4elav.PU rescues mitochondrial morphology in Drp11/Drp12 flies.

    Lethality of Drp12 and Drp11/Drp12 rescued by a genomic rescue construct spanning the 'CG3210' annotation.

    Images (0)
    Mutant
    Wild-type
    Stocks (1)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (4)
    References (21)