An accidental discovery
Experts were able to prolong the life of worms
German molecular biologists accidentally extended the life of nematode worms for several days with the help of gene therapy, which slowed down the process of assembling new matrix RNA molecules. The work was published in the journal Nature (Huang et al., Decreased spliceosome fidelity and egl-8 intron retention inhibit mTORC1 signaling to promote longevity). The results were reported by the press service of the Institute of Aging Biology in Cologne.
"We found out that the PUF60 gene, which is responsible for processing the collected RNA chains, also affects the lifespan of nematodes. Mutations in this section of DNA reduce the accuracy of the assembly of new RNA molecules, which, paradoxically, prolongs the life of worms, and does not shorten it," said Huang Wenming, a researcher at MPIfBdA, whose words are quoted by the press service of the institute.
Scientists believe that the aging of the body of humans and animals is absolutely random in nature, it occurs by itself as a result of the accumulation of mutations and accidental breakdowns in cells. As recent experiments by scientists from the University of Rochester (USA) have shown, cleaning the body of worms from damaged cells with the help of gene therapy significantly prolonged their life.
Huang Wenming and his colleagues have identified another genetic mechanism that allows nematode worms to prolong their lives. They made this discovery during experiments with DNA regions that control the assembly of new strands of so-called matrix RNA. This is what scientists call sets of nucleotides, which are "working" copies of genes used for the production of various proteins.
Longevity and enzymes
As biologists explain, one of the key stages of this process is the phase in which enzymes remove so-called introns from the RNA copies of a gene. This is what researchers call fragments of "junk DNA" that are embedded between significant sections of genes as a result of self-multiplication of such meaningless segments of the genetic code.
German biologists became interested in how the quality of "cutting out" such segments from the strands of matrix RNA affects the lifespan of multicellular animals. To answer this question, the researchers introduced random mutations in the PUF60 gene, which plays a role in clearing RNA from introns, and tracked changes in the lifespan of nematode worms of the Caenorhabditis elegans species.
Subsequent observations showed that a decrease in the activity of the PUF60 gene led not to a decrease, but to an increase in the lifespan of nematodes. As scientists suggest, this was due to the fact that slowing down the assembly of matrix RNA molecules led to a decrease in the activity of genes from the mTORC chain, which plays an important role in controlling the processes of growth and vital activity of cells.
Why these shifts led to the prolongation of life, scientists cannot yet say, but they hope that subsequent experiments on nematodes and other model animals will help to find an answer to this question. In the long term, controlling the activity of the PUF60 gene and other DNA sites associated with the production of RNA and the activity of the mTORC chain will make it possible to prolong human life, Hong Wenming and his colleagues summed up.
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