Mitochondrial translation has been shown to have a significant impact on stress resistance and cellular lifespan in research published today in Cell Metabolism. The discovery, made in yeast cells, is the result of a collaboration among five research groups at the University of Stockholm and Gothenburg. The team found that decreased accuracy of mitochondrial translation shortened chronological lifespan and increased accuracy extended lifespan.
They also reported that cytosolic protein homeostasis and nuclear stress signaling are controlled by mitochondrial translation efficiency in an inter-connected organelle quality control network.
Previous research has shown that in aging cells, various organelles stop functioning one after the other. Because the organelles are coordinated to counteract damage to proteins that occur in cells, their interdependencies are of great importance for aging and health.
The new study lead by Martin Ott, professor at Stockholm University, showed that it is production of mitochondrial proteins that controls the well being of the whole cell via previously unknown communication links. When mitochondria are exposed to stress, a protection program is activated to keep all the functions of the cell in check, a mechanism that also operates when cells age. Importantly, the study shows that in aging cells, this communication between the organelles collapses, which causes vital cellular functions to deteriorate or fail.
"What we now want to investigate is when, how and why communication between cellular organelles ceases to function during aging," says Claes Andréasson, a lecturer at Stockholm University and a senior author of the study.