Mitochondria cannot autonomously cope with stress and must instead call on the cell for help. A team of molecular geneticists led by Lucas Jae have identified the long-sought signaling pathway which enables the organelles to do so.
Illustration: Olga Ziegemann
Mitochondria are membrane-bounded intracellular organelles that supply the energy needed to power the biochemical operations required for cell function and survival. The energy is provided in the form of a compound called ATP, which can be hydrolyzed by specific enzymes to drive chemical reactions. When mitochondria are subjected to stress – owing to the accumulation of misfolded proteins, for example – their functional capacities are diminished. Degradation of mitochondrial function can have serious consequences for the affected cells, and potentially for the whole organism. In order to activate protective measures, mitochondria must transmit a distress signal into the surrounding cytosol. In a paper that appears in the leading scientific journal Nature, researchers led by Professor Lucas Jae at the LMU Gene Center now report that they have characterized the elusive signaling pathway that triggers the response to mitochondrial stress in human cells. Mitochondrial dysfunction is at the root of many serious disorders, and functional deterioration of these organelles is regarded as a major component of the aging process. The new findings are therefore of considerable significance in the search for new therapeutic approaches to the treatment of age-related diseases.
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A pathway coordinated by DELE1 relays mitochondrial stress to the cytosol.
Fessler E, Eckl EM, Schmitt S, Mancilla IA, Meyer-Bender MF , Hanf M, Philippou-Massier J, Krebs S, Zischka H & Jae LT.
Nature. 2020 Mar 19; 579(7799) doi: 10.1038/s41586-020-2076-4