D-20
Chronobiology
Exploring the link between neuronal mitochondrial DNA damage and sleep
Marina Propato-Lots1,2, Agustina Bruno-Vignolo1,3, Canela Pedreira-Gonzalez1,3, Emiliano Kalesnik-Vissio1,3, Nara I. Muraro1
1. Biomedicine Research Institute of Buenos Aires-CONICET-Partner Institute of the Max Planck Society. Godoy Cruz 2390, C1425FQD, Buenos Aires, Argentina.
2. Biological Sciences Student of the Faculty of Exact and Natural Sciences, University of Buenos Aires, Argentina.
3. PhD program of the Faculty of Exact and Natural Sciences, University of Buenos Aires, Argentina.
Presenting Author:
mpropatol@gmail.com
Sleep is a highly conserved biological process whose function remains under intense investigation. Recent evidence suggests that the repair of DNA damage accumulated during wakefulness is a key component of sleep regulation. While nuclear DNA damage has been linked to sleep homeostasis, the role of mitochondrial DNA (mtDNA), particularly vulnerable to oxidative stress, remains largely unexplored. This project aims to determine whether neuronal mtDNA damage acts as a cellular stress signal capable of modifying sleep regulation in Drosophila melanogaster. By addressing whether mtDNA integrity contributes to sleep homeostasis, this study will provide novel insights into the link between genomic stability and physiological regulation of sleep. The findings may help clarify how mitochondrial dysfunction contributes to neuronal vulnerability and sleep-related pathologies.