Cologne, Germany: In the latest study published by the Max Planck Institute for Biology of Ageing, Dr. Wenming Huang, a Max Planck scientist, and his team have revealed that they have identified a new gene mutation that has promising applications for aging research.

RNA is a key cellular transmitter and serves as a blueprint for protein synthesis. Newly synthesized RNA undergoes processing, during which introns are eliminated to yield mature mRNA, which codes for the protein. Splicing is the process of separating these segments, and the spliceosome is the part of the cell that controls it. The study concluded that faulty RNA processing can extend the human lifespan.

Discovery of Long-lived worms called PUF60

According to Dr. Wenming Huang, a Max Planck scientist, “We found a gene in worms, called PUF60, that is involved in RNA splicing and regulates life span.”

RNAs containing this gene’s mutations retained introns due to faulty splicing. It followed that this RNA’s ability to translate into fewer of its target proteins was compromised. Worms with the PUF60 gene mutation unexpectedly lived far longer than their non-mutated counterparts.

A number of proteins involved in the mTOR aging pathway were particularly vulnerable to this malfunction in synthesis. This key regulator of cellular metabolism also acts as a sensor for food availability. For a long time, scientists have been interested in it as a possible therapeutic target for slowing down the aging process. Researchers have also shown that when PUF60 activity is slowed down in human cell cultures, mTOR signaling pathway activity goes down.

PUF60 mutation in Humans

Mr. Adam Antebi, who is the director of the Max Planck Institute and oversaw the research, highlighted that, “We think that by changing what happens to introns in RNAs, we have found a new way to control how mTOR signals and how long a cell lives.” Interestingly, there are also human patients with similar mutations in the PUF60 gene. These patients have growth defects and neurodevelopmental disorders. Perhaps in the future, these patients could be helped by administering drugs that control mTOR activity. But of course, this needs more research.”

The Max Planck Society provided funding for the study.

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