The secret is in the mitochondria
The main secret of longevity has been found in mitochondria
Scientists at the Max Planck Institute for the Biology of Aging in Germany have identified a new mechanism of aging associated with mitochondria and lysosomes. The results of the study help explain why mitochondrial functions deteriorate with age not only in mammals, including humans, but also in many other animals. The researchers' article revealing the main secret of long life was published in the journal Nature Metabolism (Tharyan et al., NFYB-1 regulates mitochondrial function and longevity via lysosomal prosaposin).
It is known that mitochondria not only provide the cell with energy in the form of ATP molecules, but also play an important and complex role in the aging process. With age, the effectiveness of mitochondria decreases, which is associated with inflammatory reactions, however, on the other hand, a moderate decrease in the activity of organelles can stimulate protective reactions that contribute to longevity. In mammals, mitochondrial functions are regulated by a number of regulatory molecules (PGC-1a, YY1 and NRF10), but these factors are absent in invertebrates.
To determine the mechanisms controlling the functions of mitochondria common to multicellular ones, scientists conducted a genetic screening of regulatory molecules in a model nematode Caenorhabditis elegans. To do this, they induced reproductive diapause in adult worms – a long-term state of rest that occurs during starvation. During diapause, physiology and metabolism are rebuilt. The researchers were interested in which molecules, upon exiting this state, affect the cco-1 gene encoding cytochrome c oxidase (complex IV), an important component of mitochondria involved in cellular respiration.
Scientists used the method of RNA interference, in which small RNA molecules embedded in the body suppress the activity of various regulatory molecules: transcription factors, cell nucleus receptors, chromatin regulators (substances of the cell nucleus) and enzymes, including phosphatases and kinases. In total, 30 candidate molecules affecting the activity of cco-1 were identified.
One of the most important roles is played by the nuclear transcription factor NFYB-1, which is a component (subunit) of the transcription complex. Suppression of NFYB-1 leads to disruption of mitochondrial gene activity, reduction of oxygen consumption, destruction of mitochondria and shortening of the life span of the model organism.
The researchers found out that the transcription factor controls another protein – prosaposin. This compound is localized in lysosomes, where the destruction and processing of molecules occurs. If you limit the activity of prosaposin, then mitochondria, on the contrary, restore their functions, and the life span increases. A similar effect occurs with the addition of cardiolipin, an important component of the inner membrane of mitochondria, with which prosaposin interacts.
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