Increased interaction between endoplasmic reticulum and mitochondria following sleep deprivation

• DOI: 10.1186/s12915-022-01498-7
• Publication Date: 2023-01-04T18:02:51Z
• Authors: Amina Aboufares E...; Edgar Buhl; Sabrina Galizia; James J. L. Hodge; Luisa de Vivo; Michele Bellesi
• Keywords: Proteostasis; Homeostasis; Calcium Signaling

Abstract Background Prolonged cellular activity may overload cell function, leading to high rates of protein synthesis and accumulation misfolded or unassembled proteins, which cause endoplasmic reticulum (ER) stress activate the unfolded response (UPR) re-establish normal homeostasis. Previous molecular work has demonstrated that sleep deprivation (SD) leads ER in neurons, with a number ER-specific proteins being upregulated maintain optimal proteostasis. It is still not clear processes activated by lead ER- stress, but increased metabolism, higher request for synthesis, over production oxygen radicals have been proposed as potential contributing factors. Here, we investigate transcriptional ultrastructural mitochondrial modifications induced loss. Results We used gene expression analysis mouse forebrains show SD was associated significant genes involved also ER-mitochondria interaction, calcium homeostasis, respiratory activity. Using electron microscopy, showed general increase density cisternae pyramidal neurons motor cortex. Moreover, established new contact sites mitochondria, so-called mitochondria membranes (MAMs), important hubs molecule shuttling, such lipids, modulation ATP redox state. Finally, Drosophila male mutant flies (elav > linker), MAMs had genetically increased, reduction amount consolidation without alterations homeostatic SD. Conclusions provide evidence loss induces characterized crosstalk between mitochondria. formation could represent key phenomenon multiple ensure appropriate responses metabolism. In addition, establishment play role regulation under baseline conditions.