Researchers from the Max Planck Institute for Biology of Aging in Cologne have discovered that controlling RNA metabolism is critical for regulating animal longevity. They found that worms live longer when certain RNAs are processed differently during RNA maturation. This may be an additional way for organisms to control the aging process.
RNA is an important carrier of information in our cells and serves as a blueprint for the production of proteins. When the newly formed RNA is processed, the so-called introns are cut to produce the mature mRNA coding for the protein. This cut is called “braiding” and is controlled by a compound called “braiding”.
We found the gene in wormscalled PUF60, is involved in RNA splicing and regulation OmarMax Planck scientist Dr. Wenming Huang, who made the discovery, says. Mutations in this gene cause imprecise splicing and retention of introns within specific RNAs. As a result, smaller amounts of the corresponding proteins were formed from this RNA. Surprisingly, worms that carry this mutation in the PUF60 gene live much longer than normal worms.
Particularly affected by this defective production were some proteins that play a role in the mTOR signaling pathway. This signaling pathway is an important sensor of food availability and serves as a control center for cell metabolism. It has long been the focus of aging research as a target for potential anti-aging drugs. The researchers were also able to show that decreased levels of PUF60 activity resulted in decreased activity of the mTOR signaling pathway in human cell cultures.
PUF60 mutation in humans
says Adam Antibe, director of Max Planck, who led the study published in aging nature.
“It is interesting that there are also human patients with the like mutations in the PUF60 gene. These patients have developmental defects and Neurodevelopmental disorders. Perhaps in the future, these patients could be helped by giving drugs that control mTOR activity. But of course, this needs more research.”
Wenming Huang et al, Decreased particle splicing resolution and egl-8 intron retention inhibit mTORC1 signaling to enhance longevity, aging nature (2022). DOI: 10.1038 / s43587-022-00275-z
Max Planck Society
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