An insertion of P{EP} at 29bp 5' to the park transcriptional start site, generated by mobilising P{EP}parkP30, which is still present.
parkP21 mutants display a prominent defect in the rapid phase of cytoplasm transfer from the nurse cells to the oocyte during oogenesis. Nurse cells fail to regress and persist until the completion of oogenesis. At the end of oogenesis, the mature egg is a cup-like shape and displays a strong reduction in size.
Homozygotes have an abnormal wing posture phenotype, which increases in frequency with age. The mutant adults also show progressive loss in climbing ability and are shorter lived than normal.
Mitochondria in the indirect flight muscles of mutant adults have an elongated morphology.
parkP21 has abnormal locomotor behavior phenotype, enhanceable by Pgam5UAS.cIa/Scer\GAL4da.PU
parkP21 has short lived phenotype, enhanceable by Pgam5UAS.cIa/Scer\GAL4da.PU
parkP21 has visible phenotype, non-suppressible by Pgam5NP0568
parkP21 has abnormal locomotor behavior phenotype, non-suppressible by Pgam5NP0568
parkP21 has short lived phenotype, non-suppressible by Pgam5NP0568
parkP21 has mitochondrion phenotype, suppressible by Pgam5NP0568
parkP21 has wing phenotype, non-suppressible by Pgam5NP0568
Pgam5NP0568 has little effect on the abnormal wing posture phenotype of parkP21 flies, and fails to rescue the progressive loss in climbing ability and reduced lifespan of parkP21 flies.
Expression of Pgam5Scer\UAS.cIa under the control of Scer\GAL4da.G32 enhances both the progressive loss in climbing ability and reduction in lifespan seen in parkP21 flies.
The elongated morphology of the mitochondria in the indirect flight muscles of parkP21 adults is suppressed by Pgam5NP0568.