Researchers at Oxford University conducted an important study on the Drosophila (fruit flies) in order to understand the biological importance of sleep. As a result, they discovered that sleep deprivation directly challenges the function of mitochondria, which are the energy centers of the brain.
This study, which is published in Nature, shows that sleep drive is connected to an electron imbalance in the brain’s energy production centers. Researchers analyzed genetic profiles of rested and sleep-deprived flies at a single-cell level. After sleep deprivation, genes that are responsible for mitochondrial respiration and ATP synthesis are seen to be quite active in neurons from the dorsal fan-shaped body (dFBN) in the brain; the region is responsible for sleep management.
Some of the findings about the relation between mitochondria and sleep deprivation are really notable, because this situation directly affects the biological processes related to cellular energy metabolism. Sleep deprivation increases mitochondrial fragmentation in some neurons, thus enabling rapid clearance of damaged parts. Hence, the cell maintains its structural integrity while trying to preserve efficiency in energy production.
Moreover, increasing energy needs result in an increase in the number of contact areas between mitochondria and endoplasmic reticulum. These contact regions facilitate lipid and calcium exchange and so play a critical role in the management of energy metabolism. Therefore, the sleep deprivation not only alters mitochondrial morphology but also reshapes the inter-organelle communication.
Sleep acts as a repairing mechanism in balancing these processes. It has the capacity to reverse the structural changes in mitochondria that resulted from sleep deprivation. Experimental evidence shows that mitochondrial dynamics play a critical role in sleep patterns: experimental induction of mitochondrial fusion increases the sleep duration and depth, while fragmentation decreases the duration. These insights indicate that there is a reciprocal relationship between sleep and mitochondrial integrity, and mitochondrial dynamics are one of the biological markers of the need for sleep.
Researchers think that dFBN neurons are less active while awake, and this leads to the filling of ATP stores, the excess of electrons in mitochondria, and the generation of reactive oxygen species (ROS). This ROS accumulation serves as a biological signal for sleep need.
Collected data shows that sleep supports an older metabolic need in addition to memory consolidation. As suggested by researchers, sleep becomes important to balance the energy metabolism when the oxygen-dependent nervous systems begin to evolve. In this context, Prof. Gero Miesenböck highlights the main idea of the research by his words: “Sleep, as with hunger, may be a fundamental biological drive that has its origins in cellular energy regulation. Our mitochondria work as an inner chronometer, which decides when we need to sleep.”
This study serves as an indicator that future approaches targeting mitochondrial function in the treatment of sleep disorders will continue to emerge.
Author: Alper Demirezen
Editor: Şimal Yıldız
Reference: Sarnataro, R., Velasco, C.D., Monaco, N. et al. Mitochondrial origins of the pressure to sleep. Nature (2025). https://doi.org/10.1038/s41586-025-09261-y
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