Scientists found that worms live longer if introns stay in particular RNAs.
The study found that faulty RNA processing can result in longer life..
RNA is a crucial info transmitter in our cells and acts as a blueprint for protein production. When freshly formed RNA is processed, introns are gotten rid of to produce mature mRNA coding for protein. This cutting is referred to as “splicing,” and it is controlled by a complex called the “spliceosome.”.
Long-lived worms.
” We found a gene in worms, called PUF60, that is associated with RNA splicing and regulates life period,” says Max Planck scientist Dr. Wenming Huang who made the discovery.
This genes mutations led to incorrect splicing and the retention of introns within particular RNAs. As an outcome, less of the corresponding proteins were produced from this RNA. Remarkably, worms with the PUF60 gene mutation endured substantially longer than normal worms.
The roundworm Caenorhabditis elegans is an important model organism in aging research. The worm in the image is identified with GFP:: RNP-6. Credit: Max Planck Institute for Biology of Ageing.
Particularly affected by this malfunctioning production were some proteins that play a function in the mTOR signalling pathway. This signalling path is a crucial sensing unit for the accessibility of food and serves as a control centre of cell metabolism. It has actually long been the focus of ageing research as a target of possible anti-ageing drugs. The researchers were also able to display in human cell cultures that lowered levels of PUF60 activity led to lower activity of the mTOR signalling pathway.
PUF60 anomaly in people.
” We believe that by altering the fate of introns in RNAs, we have actually discovered an unique system that manages mTOR signaling and longevity,” states Max Planck Director Adam Antebi who led the study. “Interestingly, there are also human patients with similar anomalies in the PUF60 gene. These patients have growth flaws and neurodevelopmental conditions. Possibly in the future, these patients might be assisted by administering drugs that control mTOR activity. But of course, this needs more research.”.
Reference: “Decreased spliceosome fidelity and egl-8 intron retention hinder mTORC1 signaling to promote durability” 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 research study was funded by the Max Planck Society.
RNA is a crucial information transmitter in our cells and acts as a blueprint for protein production. This genes mutations resulted in inaccurate splicing and the retention of introns within specific RNAs. As an outcome, less of the matching proteins were produced from this RNA.” We believe that by altering the fate of introns in RNAs, we have actually discovered an unique system that controls mTOR signaling and durability,” states Max Planck Director Adam Antebi who led the research study.