Ageing has long been perceived as an inevitable, unregulated process leading to the accumulation of cellular damage and ultimately, the decline of our bodies. However, in 1993, a groundbreaking discovery challenged this notion. Researchers identified a mutation in a single gene that doubled the lifespan of a worm, pointing to the idea that specific genes play a crucial role in regulating ageing. Since then, ongoing research has delved into the molecular intricacies of ageing, leading to surprising revelations.
Recently, a series of papers have shed light on a novel biochemical pathway that regulates ageing. This pathway relies on signals exchanged between mitochondria, the powerhouse of the cell.
Certain discoveries were detailed in Science Advances, while additional findings were shared on the scientific preprint server.
Conducting experiments with worms, researchers observed that damage to mitochondria in brain cells initiated a repair response, which then spread throughout the organism, extending its lifespan by 50%.
Surprisingly, cells in the germline, responsible for producing eggs and sperm, played a central role in this anti-ageing communication system. This finding adds new dimensions to the discussion of ageing and the biological clock, emphasising the importance of intercellular communication in regulating lifespan.
Recent research builds upon the idea that mitochondria, traditionally viewed as the cell’s powerhouse, are also social organelles capable of communication. This communication occurs not only within the same tissue but across different tissues in the body.
A decade ago, cell biologist Andrew Dillin discovered hints of this novel pathway while investigating life-extending genes in worms. Surprisingly, damaging the mitochondria extended the worms’ lives by 50%, with the effect being driven by damaged mitochondria in the nervous system. Further research revealed that a repair response, known as the unfolded protein response, was activated in various tissues, even when their mitochondria were intact.
To understand how the unfolded protein response was communicated throughout the organism, Dillin’s team discovered that stressed neurons used vesicles to carry a signal called Wnt beyond nerve cells. Wnt signalling, known for its role in embryonic development, triggers repair processes like the unfolded protein response. The researchers found a gene expressed only in germline mitochondrial that could interrupt Wnt’s developmental processes, highlighting the critical role of germline cells in transmitting signals between the nervous system and other tissues.
While the study focuses on worms, its findings suggest potential parallels in more complex organisms like humans. As worms age, the quality of their eggs or sperm declines, leading to a decrease in the transmission of signals from the brain’s mitochondria. This decline in signalling efficiency correlates with the ageing process in the rest of the organism. Although the direct application to humans remains uncertain, the hypothesis aligns with an evolutionary perspective: as long as germ cells are healthy, they send pro-survival signals; as their quality declines, there may be no evolutionary reason to extend lifespan further.
The ability of mitochondria to communicate among themselves is attributed to their ancient origins as free-living bacteria that joined forces with primitive cells.
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