A mutation in worms may lead to a longer life

A genetic mutation has been linked to longer-lived worms by scientists at the Max Planck Institute in Munich Germany.

Their study found that faulty RNA processing can result in longer life

The roundworm Caenorhabditis elegans is an important model organism in ageing research. The worm in the image is labelled with GFP::RNP-6. © Max Planck Institute for Biology of Ageing

RNA transmits information in cells and acts as a blueprint for protein production. When freshly formed RNA is processed, introns are removed to produce mature mRNA coding for protein. Introns are noncoding sections of an RNA transcript, or the DNA encoding it. They are spliced out before the RNA molecule is translated into a protein. 

The researchers found that one gene, called PUF60, is involved in RNA splicing and regulates lifespan.

When the gene mutates, it can cause inaccurate splicing and intron retention within certain RNAs. Because of this, the affected RNA produced less of the corresponding proteins. Worms with this PUF60 gene mutation had more introns in their RNA and lived longer than normal worms.

Researchers found the defective production affected some proteins that play a role in the mTOR signaling pathway, an important sensor for the availability of food and a control center for cell metabolism.  

Longevity scientists have long focused on this signaling pathway as a target of potential anti-aging drugs.

Working with human cell clusters, the researchers showed that reduced levels of PUF60 activity led to lower activity of the mTOR signaling pathway in people, too.

“We think that by altering the fate of introns in RNAs, we have discovered a novel mechanism that regulates mTOR signaling and longevity,” Max Planck Director Adam Antebi, who led the study, told the Max Planck Society.

Antebi suspects the findings may lead to extending human lifespan.

“Interestingly, there are also human patients with similar mutations in the PUF60 gene,” he said. “These patients have growth defects and neurodevelopmental disorders. Perhaps in the future, these patients could be helped by administering drugs that control mTOR activity.” 

More research is necessary, but the promise of the research is fascinating.