CM – Cellular Aging: A Fundamental Paradox Solved

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November 9, 2021

from the University of Montreal Hospital Research Center (CRCHUM)

In a study published in Nucleic Acids Research, the team of cancer researcher Francis Rodier, professor at the Université de Montréal, shows for the first time that the cellular senescence that occurs when aging cells stop to divide is caused by irreversible damage to the genome, rather than simply telomere erosion.

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This discovery contradicts the most widespread scientific model in the last 15 years, which is based on one principle: telomeres, caps at the ends of chromosomes, which are supposed to protect the genetic information, erode with every cell division. If they get too short, they tell the cell not to divide anymore, thus preventing damage to its DNA. When dormant, the cell enters senescence.

For this model to be valid, inactivation of a single telomere should be sufficient to activate the senescence program. Rodier’s laboratory and many others had already observed that several dysfunctional telomeres are necessary.

« Most surprisingly, the cells divide one last time before they really enter senescence, » says Rodier. “In fact, the cell division caused by telomere dysfunction is so unstable that it creates genetic defects. Contrary to what is thought, senescent cells have an abnormal genome. We show that in our study. ”

In order to achieve such results, Rodier’s research team was able to count on the most modern imaging equipment financed by the Institut du Cancer deMontréal.

Reproduce in the laboratory and make all telomeres of a cell population become dysfunctional, ”says Ph.D. Student Marc-Alexandre Olivier, co-first author of the study with former colleague Sabrina Ghadaouia, currently a postdoc in England. “With our equipment, we then observed in real time what was happening in each individual cell.”

Over time, senescent cells build up in the body and are responsible for the development of diseases such as cancer. This study therefore opens up new research opportunities.

Could telomeres, for example, be repaired before the senescence phase, thereby preventing cell aging and genomic instability? The scientific community has been discussing this potential cell rejuvenation for several years. However, these new therapeutic approaches still require fine-tuning.

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