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Researchers Have Discovered a Mutation That Significantly Increases Lifespan

Scientists found that worms live longer if introns remain in certain RNAs.

The study found that faulty RNA processing can result in longer life. 

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Ribonucleic acid (RNA) is a polymeric molecule similar to DNA that is essential in various biological roles in coding, decoding, regulation and expression of genes. Both are nucleic acids, but unlike DNA, RNA is single-stranded. An RNA strand has a backbone made of alternating sugar (ribose) and phosphate groups. Attached to each sugar is one of four bases—adenine (A), uracil (U), cytosine (C), or guanine (G). Different types of RNA exist in the cell: messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA).

” data-gt-translate-attributes='[{“attribute”:”data-cmtooltip”, “format”:”html”}]’>RNA is an important information transmitter in our 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. This cutting is known as “splicing,” and it is controlled by a complex known as the “spliceosome.”

Long-lived worms

“We found a gene in worms, called PUF60, that is involved in RNA splicing and regulates life span,” says Max Planck scientist Dr. Wenming Huang who made the discovery.

This gene’s mutations resulted in inaccurate splicing and the retention of introns within certain RNAs. As a result, less of the corresponding proteins were produced from this RNA. Surprisingly, worms with the PUF60 gene mutation survived significantly longer than normal worms.

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

Particularly affected by this defective production were some proteins that play a role in the mTOR signalling pathway. This signalling pathway is an important sensor for the availability of food and serves as a control centre of cell metabolism. It has long been the focus of ageing research as a target of potential anti-ageing drugs. The researchers were also able to show in human cell cultures that reduced levels of PUF60 activity led to lower activity of the mTOR signalling pathway.

PUF60 mutation in humans

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

Reference: “Decreased spliceosome fidelity and egl-8 intron retention inhibit mTORC1 signaling to promote longevity” by Wenming Huang, Chun Kew, Stephanie de Alcantara Fernandes, Anna Löhrke, Lynn Han, Constantinos Demetriades and Adam Antebi, 19 September 2022, Nature Aging
DOI: 10.1038/s43587-022-00275-z

The study was funded by the Max Planck Society.

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