TORC1 links chromosome errors to cell growth
Errors in how chromosomes are divided during cell division seem unrelated to metabolism. But new research in eLife shows these two processes are directly connected, through a molecular switch long known as a regulator of ageing.
When a cell divides, chromosomes must be distributed equally between the two daughter cells. When that goes wrong, cells end up with too much or too little genetic material. These errors are known as chromosome segregation defects. They are associated with cancer, accelerated ageing and cell death.
Then there is TORC1 (Target of Rapamycin Complex 1): a protein complex that integrates environmental signals to regulate cell growth, metabolism and lifespan. TORC1 is one of the most studied mechanisms in longevity science. Inhibiting it, for example with rapamycin, extends lifespan in multiple organisms.
The study, published in eLife, demonstrates for the first time that TORC1 and the proteins that hold chromosomes together (cohesin) communicate with each other. Disruptions in cohesin influence TORC1 activity, and vice versa.
Cohesin and its role in ageing
Cohesin is a protein complex that holds two sister chromatids (identical copies of a chromosome after replication) together until the cell is ready to divide them. Errors in cohesin lead to segregation defects. With age, the accuracy of cohesin declines, which partly explains why chromosome errors become more common in older cells.
Linking cohesin to TORC1 adds a new dimension. It suggests that disruptions in a cell’s nutrient and growth signals can also affect chromosome stability. Conversely, maintaining cohesin function may also support a healthier TORC1 profile.
What this means
For longevity science, this is a significant connection. Two processes each independently associated with ageing turn out to communicate with each other. That raises the possibility that interventions targeting TORC1 could indirectly influence chromosome stability as well. Further research is needed to determine whether this mechanism operates the same way in mammalian cells.