the Scientists of the Institute of aging biology of the max Planck Society in Germany have identified a new mechanism of aging that is associated with the mitochondria and lysosomes. The results of the study help to explain why mitochondrial function deteriorates with age in mammals, including humans, but many other animals. Article researchers, revealing the secret of long life, published in the journal Nature Metabolism.

it is Known that mitochondria not only provide cells with energy in form of ATP molecules, but also play an important and complex role in the aging process. With age, mitochondrial efficiency decreases, which is associated with inflammatory reactions, but, on the other hand, a moderate decrease in the activity of the organelles can stimulate a protective response that promotes longevity. In mammals, mitochondrial function regulates a number of regulatory molecules (PGC-1A, YY1 and NRF10), but invertebrates these factors do not exist.

to determine the mechanisms controlling mitochondrial function, are common to metazoans, scientists have conducted genetic screening of regulatory molecules from the model nematode Caenorhabditis elegans. To do this, they have caused the adult worms reproductive diapause, a long — term quiescent state occurring in starvation. During diapause rebuilds physiology and metabolism. Researchers were interested in which molecules upon exit from this state will affect gene cco-1, encoding the cytochrome C oxidase (complex IV) — an important component of mitochondria that participates in cellular respiration.

the Scientists used a technique called RNA interference in which small RNA molecules introduced into the body, inhibit the activity of various regulatory molecules: transcription factors, receptors the nucleus of our cells, regulators of chromatin (the substance of the cell nucleus), and enzymes, including the phosphatase and kinase. Just was 30 molecules candidates that affect the activity of cco-1.

One of the most important roles is played by the nuclear transcription factor, NFYB-1, which is a component (subunit) transcription complex. Suppression NFYB-1 leads to disruption of the activity of mitochondrial genes, reduced oxygen consumption, destruction of mitochondria and reduced life expectancy model organism.

the Researchers found that a transcription factor controls another protein — prosaposin. This compound is localized in the lysosomes, where the destruction and recycling of molecules. If you limit the activity prosaposin, the mitochondria, on the contrary, restore its function, and the lifetime increases. A similar effect occurs when adding cardiolipin is an important component of the inner mitochondrial membrane, which interacts with prosaposin.