Transcription repressor that inhibits transcription of srl/PGC-1-alpha to negatively regulate mitochondrial biogenesis and thereby promotes neurodegeneration (PubMed:27819722, PubMed:32138754). In neurons, functions downstream of the Pink1-park pathway and is likely to act as part of the Pink1-park homeostatic mechanism that maintains mitochondrial quality and function through degradation (mitophagy) and synthesis (biogenesis) (PubMed:32138754). Interacts with park. Phosphorylated by Pink1 leading to ubiquitination by park. Ubiquitinated by park. Polyubiquitination by park leads to degradation by the proteasome which likely activates mitochondrial biogenesis to maintain neuron health and function. RNAi-mediated knockdown in dopamine neurons increases dopaminergic mRNA levels of srl and its downstream transcription factors ewg and TFAM, and also results in a significant increase in mean lifespan (64 days) compared to controls (60 days) (PubMed:27819722, PubMed:32138754). However, it has no effect on mitochondrial abundance, neuronal survival or climbing performance (PubMed:32138754). Double knockdown with park or Pink1 in the dopamine neurons, improves climbing performance defects and rescues decreased mRNA levels of srl, ewg and TFAM in the single park or Pink1 mutants (PubMed:32138754). RNAi-mediated knockdown in the eye has no significant effect on ommatidia or bristle number (PubMed:32138754).