Scientists have discovered a very subtle twist in the genetics of senescent cells. This seems to make it less and less functional over time.
R.Researchers at Northwestern University revealed As animals such as mice, rats, medaka, and even humans age, the balance of long and short genes gradually deteriorates in virtually every cell in the body.
This finding suggests that there are no specific genes controlling the aging process. Instead, old age appears to be governed by system-level changes with complex effects.And this can affect thousands of different genes and their respective proteins.
However, for individual genes, the changes are so small that they are insignificant. That’s probably why they’ve slipped past our notices until now.
“We are mainly looking at a small number of genes, and we think some of them can explain the disease. To tell Northwestern University Data scientist Luis Amaral.
“So maybe we weren’t focusing on the right things before. Now that we have this new understanding, it’s like having a new instrument. We’re looking at space with a telescope.” It’s like Galileo: looking at genetic activity through this new lens allows us to look at biological phenomena in a different way.”
Typically, in individual cells or groups of cells, the code represented by DNA is translated into RNA, known as a free-running set of instructions. transcriptome.
This mobile library of genetic recipes is what cells use to create their parts and perform various functions. The contents also seem to change over time.
In healthy young animals, the activity of short and long genes is balanced across the transcriptome, and this balance is carefully monitored and maintained. However, as individuals age, short genes tend to become more dominant.
In fact, several different types of animals have been shown to proliferate short transcriptomes with age.
“Changes in gene activity are very small, and thousands of genes are involved in these small changes. I will explain Developmental biologist Thomas Stoger.
“We found this change to be consistent across different tissues and across different animals. It was found almost everywhere. A single, relatively simple principle explains the gene activity that occurs in animals. It’s very elegant that it seems to explain almost all of the changes in life as they get older.”
Similar to the process of aging itself, the transition to a smaller transcriptome begins early and is gradual.
In rats, tissue samples taken at 4 months of age had relatively longer median gene lengths than those taken at 9 months of age.
Similar transcriptome changes were observed in medaka from 5 to 39 weeks of age.
To test the pattern in humans, researchers genotype-tissue expression The (GTEx) project publishes genetic information collected from approximately 1,000 deceased individuals.
Among humans, transcriptome length was again found to be a predictor of old age, becoming important in the 50-69 year old group.
Compared with the younger group aged 30–49 years, the older group showed longer transcripts that were less likely to “fold” or be functionally activated compared to the shorter ones.
“The human results are very strong because we have more human samples than other animals.” To tell Amaral.
“It’s also interesting to note that while all mice we studied were genetically identical, of the same sex, and bred in the same laboratory conditions, humans were all different. They all differed for different reasons.” died at age. We analyzed samples from males and females separately and found the same pattern.”
Still unsatisfied with the results, researchers at Northwestern University next investigated some anti-aging effects. intervention About transcriptome length. The majority of interventions favored long transcripts despite differing effects on the body.
The authors conclude that aging cannot be reduced to a single cause of transcriptome imbalance.
Instead they quarrel Its “multiple environmental and internal conditions” probably lead to short genes becoming more active in the body.
“Our findings on anti-aging interventions have inspired us to understand the direction of causal relationships between other age-dependent cellular and transcriptomic changes and length-related transcriptomic imbalances. We believe that doing so may open new research directions for anti-aging interventions,” said the authors. Conclusion.
This research natural aging.
