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.
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.