The fewer calories, the healthier the DNA
About the diet for the cell, rapamycin and life expectancy
NanoNewsNet based on the materials of Z GMBH – A Diet for the Cell: Keeping the DNA Fit with Fewer CaloriesAs a rule, cells successfully repair spontaneously damaged genetic material, but, unfortunately, the process of DNA repair is imperfect, and sometimes damaged DNA is transmitted to descendant cells.
A group of scientists from the Center for Molecular Biology of Heidelberg University (Center for Molecular Biology of Heidelberg University, Z GMBH) found that in yeast cells, the amount of nutrients can affect the mechanisms of control over DNA repair and, consequently, its quality. According to the head of the group, Dr. Brian Luke, the new data they obtained on cell biology, published in the journal Cell Reports (High Nutrient Levels and TORC1 Activity Reduce Cell Viability following Prolonged Telomere Dysfunction and Cell Cycle Arrest), may contribute to the emergence of new strategies for the development of anti-cancer drugs.
The genetic material – DNA – contains all the information necessary for the normal functioning of the cell. Every time a cell divides, this information must be copied exactly so that new cells, having received an exact copy of it, can, in turn, function properly. However, the inheritance of damaged DNA must be blocked. In order to recognize the altered DNA and prevent its transmission, cells have developed control mechanisms that stop their division. By temporarily stopping the division cycle, the cell gets more time to repair the damaged genetic material. However, in some cases, DNA cannot be effectively restored, even if the "checkpoints" are activated. If the DNA damage persists for a very long time, the cells can "turn off" the checkpoints without waiting for the DNA to be restored. This process, called adaptation, is beneficial to the cell, because it will finally be able to divide again.
"However, for the body as a whole, adaptation is often dangerous, since unrecoverable DNA can lead to diseases such as cancer," explains Dr. Luke.
Molecular biologists from his group Julia Klermund and Katharina Bender have found a way to prevent cells from disabling such checkpoints and thus increase the time during which cells can repair their DNA, thereby preventing the transmission of damaged DNA to their offspring. The researchers found that the main factor influencing this process is the amount of nutrients in the cellular environment. If cells with DNA damage are in an environment with low levels of nutrients, they do not adapt, and their division is completely stopped by a checkpoint. The same effect is observed when cells are treated with rapamycin, which suppresses the metabolic signaling pathway and, therefore, simulates a lack of nutrients.
When DNA is damaged in cells, checkpoints are activated, which stops the cellular
the cycle also gives time for the repair of genetic material. If DNA damage cannot be repaired,
a choice must be made between a long-term stop of the cell cycle and its continuation in the presence of
damage (adaptation). While a long-term shutdown jeopardizes education
clones, continued proliferation is associated with the risk of genome instability. On this choice, through the target
rapamycin TORC1 (target of rapamycin complex 1), affects metabolic signaling. Mediated by rapamycin
inhibition of TORC1 prevents adaptation of checkpoints. Preventing adaptation leads to
to increase the viability of cells and their proliferative potential (fig. Cell Reports).
"Cells in conditions with a low nutrient content turn out to be much more viable, probably because before they start dividing again, they waited for the damaged DNA to be restored," explains Klermund.
"We believe that high levels of nutrients push cells to grow and proliferate, even when they shouldn't, for example, when DNA is damaged. An environment with low levels of nutrients seems to guarantee that cells will "risk" dividing only when their DNA is fully restored," adds Dr. Luke.
Recently, scientists from the United States have demonstrated that fasting or treatment with rapamycin increases life expectancy, as well as increases the effectiveness of certain types of chemotherapeutic drugs. Dr. Luke believes that his group's study complements the data obtained in the USA with important mechanistic details of how these effects are achieved, and provides clues to further improve the effectiveness of anti-cancer drugs.
Portal "Eternal youth" http://vechnayamolodost.ru09.10.2014