An ageing cell goes through major negative changes: defective proteins are not
eliminated as they should, mitochondria – the power plants of a cell – do not function
properly, the ability to sense nutrients is lost. All of these defects lead to shortened
lifespan. One might think at first glance, they appear to have nothing to do with each
other on a molecular level. “In fact, they are highly interconnected”, says Adam Antebi,
Director at the Max Planck Institute for Biology of Ageing in Cologne. “Now we have
found a network of regulators that connects all those different cellular processes.” For
their studies the researchers used the roundworm Caenorhabditis elegans, a commonly
used model organism in the field of ageing research.
It all began with a scientific finding scientists made already some years ago:
Roundworms live much longer if you remove their germ cells – the sperm and egg
producing cells. “But we did not know why this happened”, explains Antebi. To answer
this question the scientists removed specific genes to test if these worms lost the ability
to live long. If this was the case, the researchers assumed that they found a gene that
was normally required to increase the lifespan. In the end the researchers had a list of
proteins, which extend lifetime. Many of them belonged to the so-called transcription
factors – proteins that reside in the nucleus of the cell to turn on and off other genes.
The detected transcription factors appear to work together. “We found that all these
transcription factors regulate and support one another. Actually they behave like a
network”, Antebi says. This network impacts very diverse processes in the worm-cells:
the recycling machine, the digestion system and the sensing of nutrients. “The end-result
is changes in metabolism, the process where nutrients become the fuel and building
blocks we need”, Antebi explains. With their study the researchers can begin to explain
how reproduction, metabolism and life span are intertwined.