mitochondrion & skeletal muscle of thorax
myofibril & skeletal muscle of thorax
The aberrant wing posture, thoracic indentations along with mitochondrial defects (loss of cristae) in indirect flight muscles observed in park1/parkΔ21 transheterozygous adults are all significantly rescued by Scer\GAL4Mhc.PU-driven expression of STUB1Scer\UAS.cCa, whereas their climbing ability deficit is not improved.
The reduced climbing ability of park1/parkΔ21 mutants is not exacerbated by combination with either STUB1I or STUB1II in homozygous state, but the lifespan of the double mutants is significantly decreased compared to park1/parkΔ21 single mutants.
Neither the swollen mitochondria phenotype nor the the locomotion deficit characteristic for park1 homozygous mutant third instar larvae can be suppressed by Scer\GAL4Mef2.PR-driven expression of cluUAS.Tag:MYC.
The mitochondrial morphology defects observed in larval muscles of both cluΔW and park1 homozygotes are exacerbated further in the double mutants, moreover while either cluΔW or park1 are partially lethal with about 5-10% of adult escapers, cluΔW/cluΔW;park1/park1 mutants do not yield any viable adults. On the other hand the larval locomotor deficit of either of the single mutants is not significantly worsened in the double mutants.
Expression of RetMEN2B.Scer\UAS under the control of Scer\GAL4Mef2.PR does not suppress the muscle morphology phenotype seen in the indirect flight muscles of park1/park25 mutants. The frequency of flies with "actin blobs" is decreased markedly compared to RetMEN2B.Scer\UAS expressing controls. The structural impairments seen in park1/park25 mutant mitochondria are not suppressed. The reduction in thoracic ATP levels is not rescued.
Expression of RetMEN2B.Scer\UAS under the control of Scer\GAL4Mhc.PK (limited to the pharate adult stages onwards using Scer\GAL80ts.αTub84B) does not suppress the muscle morphology phenotype seen in the indirect flight muscles of park1/park25 mutants.
Overexpression of Ucp4AScer\UAS.cWa by Scer\GAL4Act.PU reduces thoracic indentations, locomotor defects, male sterility, degeneration (cell death) and disorganization and fewer mitochondrial cristae in indirect flight muscle in park1/park1 flies.
Expression of either rictorScer\UAS.cHa or trcS292E.Scer\UAS under the control of Scer\GAL4da.PU fails to rescue the abnormal wing posture and mitochondrial aggregation phenotypes seen in park1/parkΔ21 flies.
20-day-old park1/GstO21 double mutants show significantly increased DA neuron degeneration in the PPL1 cluster compared to park1 single mutants of the same age, whereas there is no difference in neuronal degeneration between park1/GstO21 double mutants and park1 single mutants in 1-day-old flies.
Overexpression of GstO2A.Scer\UAS under the control of Scer\GAL4αTub84B.PL, a ubiquitous driver, suppresses the degeneration of IFMs in park1 mutants. Overexpression results in regular and compact muscle tissues in the dorsal longitudinal IFMs, which are similar to those of wild-type flies except for occasional vacuoles. Overexpression of GstO2A.Scer\UAS appears to prevent degeneration of the IFMs by blocking the activation of the JNK pathway and apoptosis in park1 mutants.
Expression of ATPsyn-βNIG.11154R at 18[o]C in the muscle, under the control of Scer\GAL4how-24B enhances the downturned wing and collapsed thorax phenotype found in park1 mutants, compared to park1 single mutants.
Expression of Sirt1Scer\UAS.cGa driven by Scer\GAL4arm.PU does not suppress phenotypes (collapsed thorax, downturned wings, swollen mitochondria along with increased cell death and reduced levels of mtDNA and ATP in the indirect flight muscle and locomotor defects) seen in Pink1B9/Y flies.
Expression of SNF1ATD.Scer\UAS under the control of Scer\GAL4how-24B suppresses the mitochondrial abnormalities and climbing ability defects seen in park1 mutant flies. The wing posture defects seen in park1 mutant flies are also rescued.
The defective wing and thorax phenotypes seen in park1 mutant flies are not rescued by expression of Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB. Expression of Pink1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.PB also fails to rescue the enlarged mitochondria and apoptotic muscle cells seen in adult park1 thoracic muscles.
Scer\NDI1Scer\UAS.cVa in the absence of a Scer\GAL4 driver does not suppress the sterility of park1/parkΔ21 males (even though Scer\NDI1Scer\UAS.cVa in the absence of a Scer\GAL4 driver does suppress the male sterility of Pink1B9 males).
Expression of parkScer\UAS.cSa under the control of Scer\GAL4da.PU rescues the mitochondria phenotype seen in parkΔ21/park1 mutant indirect flight muscles. The reduction in ATP levels is also rescued, and is improved to a level higher than that of controls.
Expression of parkSA.Scer\UAS under the control of Scer\GAL4da.PU fails to rescue the mitochondria phenotype seen in parkΔ21/park1 mutant indirect flight muscles. The reduction in ATP levels is rescued, and is improved to a level higher than that of controls.
Expression of parkSA.Scer\UAS under the control of Scer\GAL4Mhc.PU partially rescues the wing posture and thorax defects seen in parkΔ21/park1 mutant flies. The reduction in ATP levels is also improved.