Abstract:
Mitochondria are semi-autonomous double membrane organelle with an extrachromosomal circular DNA of approximately 19.5 kb in size and known to encodes 37 genes. Mitochondrial genome encodes 11 mRNAs which get translates to 13 polypeptides that all are subunits of oxidative phosphorylation. Ppr is a trans-acting nuclear-encoded protein which regulates post-transcriptional modification of the mitochondrial genome. During stem cell differentiation mitochondrial morphology and metabolism shift towards an increased OXPHOS activity and mitochondrial DNA content are also known to increase. Here we focused on the role of Ppr on mitochondrial DNA translation and the following effect on differentiation, using Drosophila oogenesis as a model for stem cell differentiation. We observed that Ppr is expressed in a differential manner in different stages of oogenesis and is required in an increased level in certain stages associated with Notch and EGFR signaling pathways. Depletion of ppr is resulting in clustered mitochondrial morphology and a decreased mitochondrial membrane potential, surprisingly with no evidence of energy stress. Additionally, depletion in ppr in nurse cells shows a defective oocyte nuclear migration. We observed an increased level of cytoplasmic dpERK, an EGFR read out suggesting the direct or indirect role of Ppr in EGFR signaling. Ppr mutant cells show a delay in Cut depletion with no change in NICD levels. These data together indicate a role for Ppr in maintaining mitochondrial activity and EGFR signaling in follicle cells.
