(ORDO NEWS) — Telomeres – long identical repeats found at the ends of our chromosomes – can serve as the basis for the synthesis of short peptides that play a role in disease and aging.
At the ends of chromosomes are telomeres – long repeats of six nucleotides: TTAGGG.
Due to complementary interactions with each other, these regions form loops that prevent chromosomes from sticking to each other.
However, the proteins responsible for their duplication are not able to copy the terminal DNA fragments.
Therefore, with each cell division, telomeres shorten. This process is thought to play an important role in cellular aging.
Looking at the monotonous repetition of the TTAGGG fragment, it is difficult to suspect that telomeres can carry some kind of “meaning” in terms of protein or RNA coding.
However, a new paper by Jack Griffith and colleagues challenges this conventional wisdom.
Back in 2011, it was noticed that in patients with a hereditary disease, amyotrophic lateral sclerosis, short RNA molecules are found in which six identical nucleotides are repeated.
Peptides consisting of repeats of two amino acids (valine and arginine, VR, or glycine and leucine, GL) can be synthesized on the matrix of these RNAs and play a certain role in the development of the disease.
Griffith et al drew attention to a suspicious sequence match between these RNAs and telomeres.
Biologists suggest that with aging and telomere shortening, as well as under the influence of inflammatory processes, the synthesis of VR and GL proteins can gradually increase.
In turn, accumulating, these molecules are capable of exerting a toxic effect on the cell.
Indeed, after further experimentation, the scientists found that some cancer cells contain elevated amounts of the VR protein.
The same is observed in the cells of people suffering from various diseases associated with disruption of the telomeres.
Perhaps in the future, a blood test for the presence of such proteins will be used both in medical diagnostics and as a marker of the development of aging.
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