Recently, another putative mutation that leads to early aging was discovered - in the nsd1 gene. Several dozen such genes are already known. Hypothetically, blocking these regions of the genome could slow aging and prolong life. But interference with the genome can lead to other - unpleasant consequences. However, this does not stop scientists. Experiments on disabling aging genes are now being carried out in several laboratories at once. What comes out of it.
Young old people
The first publication on the putative aging gene appeared in 1996 in the journal Science. Its authors, scientists from Japan and the USA, studied people with Werner's syndrome - in this disease, the body wears out twice as fast as usual, and a person at forty looks eighty. The researchers drew attention to a mutation in the WRN gene located on the eighth chromosome. It was assumed that because of it, some important processes in the body are disrupted, and this accelerates aging.
A few years later, the guess was partly confirmed. Only those who have two copies of the mutant WRN gene really suffer from Werner's syndrome. However, it can hardly be considered an aging gene in the literal sense: it is a mediator that affects other parts of DNA.
This is because WRN makes a protein that maintains the structure and integrity of human DNA. Any of its defects (and they are inevitable if there is a mutation in this gene) change the mechanisms of replication and restoration of the damaged molecule. This, in turn, affects the work of other regions of the genome, including those associated with aging.
Older than his years
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The gene for the melanocortin receptor type I (MC1R), recently discovered by Dutch, British and Chinese scientists, has come under suspicion. They correlated the genomes of 2,693 elderly people with the external manifestations of age reflected in their photographs.
After analyzing more than eight million single nucleotide polymorphisms - differences in the DNA sequence of only one nucleotide in size, it was established that those in the MC1R gene are associated with external signs of aging. Thus, people with two copies of the mutant MC1R variant look, on average, two years older than their actual age.
Two years seems to be a little. However, if carriers of the mutation smoke, visit tanning beds too often and lead not the most healthy lifestyle, then the gap between apparent and real age increases, the authors of the study warn.
The mutant variant of the nsd1 gene acts in a similar way. According to Canadian and British scientists, those who received a copy of it from each of the parents age faster than their peers.
Contagious aging
The CD36 gene, discovered last year by American geneticists, also plays a significant role in the aging process. Apparently, he is responsible for stopping cell division, which signals its imminent death.
While examining senescent cells, scientists noticed the unusual activity of CD36. To study it in more detail, we conducted two experiments. In the first, 15 percent of young healthy cells in culture were modified so that the CD36 gene worked more efficiently. As a result, they stopped dividing and showed clear signs of aging. Moreover, other cells in culture with a normal gene were infected with this.
In the second experiment, geneticists kept a culture of senescent cells in a nutrient solution for some time, then younger cells were placed in its place. Those, in turn, suddenly stopped sharing, as if adopting the qualities of the former "tenants". This is confirmed by experiments on fibroblasts of the skin and lungs. But why this happens is not clear, the authors of the study admit.
The gene turned off, the youth extended
Swiss scientists are experimenting with the PUM2 gene. In young cells, the protein it produces is essential for peptide synthesis. But in older people, it turns into a serious obstacle: its molecules get tangled and prevent RNA from transmitting instructions from the nucleus to those parts of the cell where proteins are collected.
Thus, one of the "victims" of PUM2 is the MFF substance, which is important for the utilization of damaged mitochondria. The fact is that the contents of these cellular energy stations, with the exception of ATP and waste products, never leave their limits. When mitochondria wear out, peculiar holes form in them, through which aggressive molecules seep into the cytoplasm of the cell, damaging the cell's DNA and causing interruptions in its work. Young cells cope with such accidents thanks to MFF, splitting mitochondria into pieces and digesting damaged fragments. In older cells, this is prevented by PUM2. As a result, cells age faster and die.
If PUM2 is turned off or cut out of DNA in time, aging will slow down, scientists suggested and blocked this gene in nematode worms. Mitochondria in all cells became younger, and animals lived significantly longer than their unmodified counterparts. But with mice, this technique was not so effective. Mitochondria have become younger only in intestinal cells.
The next step is experiments with human cell cultures. The researchers hope to find a safer way to reduce the amount of protein produced by PUM2 without genome editing.
Alfiya Enikeeva