Fig. 6: dDOR overexpression rescues while its downregulation aggravates dPINK1 mutant phenotype in drosophila flight muscles.
From: TP53INP1 exerts neuroprotection under ageing and Parkinson’s disease-related stress condition
A Living mef2-GAL4 UAS-mit::dendra2 (staining of the mitochondrial matrix) adult male dorsal longitudinal flight muscles (DLM) from control, dPINK1B9 hemizygous mutant or dPINK1B9 hemizygous mutant expressing UAS-dDOR transgenes (dDOR-F but not dDOR-L contains EcR binding motif). B Transmission electron microscopy images of adult fly thorax sections showing mitochondrial ultrastructure in DLM muscle of control, homozygous dDOR null mutant, dPINK1B9 hemizygous mutant, dPINK1B9 hemizygous mutant expressing UAS-dDOR-F and dPINK1B9 hemizygous mutant combined with homozygous dDOR null mutation. C Fly thorax sections of control, dPINK1 hemizygous mutant and dPINK1 hemizygous mutant combined with dDOR homozygous mutation stained with Toluidine blue showing DLM muscles. In dPINK1 hemizygous mutant, DLM muscles contain intact fibers that span longitudinally, as seen in the control fly. In dPINK1 hemizygous mutant combined with dDOR homozygous mutation, the extremities of DLM muscle appear ripped off from the cuticle and the muscle fibers are disorganized and torn. Four thoraces were analyzed for each condition.
