Prof Spang and her team used yeast as a model organism to investigate which processes are activated when a cell has to deal with sugar restriction. They then compared these with the response to other stress situations. It turned out that P-bodies - small cellular organelles – increase the storage of so-called mitochondrial mRNAs when experiencing sugar shortage. As mobile carriers of genetic information in the cells, mRNAs are templates for the production of vital proteins. The products of the mitochondrial mRNAs initiate an adaptation of the energy metabolism process in the power stations of the cells: the mitochondria. “This is the only way to ensure the continued survival of the cell,” explains Spang. Simultaneously, all the mRNAs that are not necessary to master the deficiency situation are degraded in the P-bodies. Until now, it was assumed that P-bodies only played a role in the degradation of mRNAs.
Furthermore, the researchers were able to identify the decision-maker responsible for this selection: “We demonstrated that the protein Puf5p primarily decides over the fate of the individual mRNA and transports it to the site where this is carried out, the P-bodies,” reports Spang. Their results have been published in the open access journal eLife.
Numerous earlier scientific investigations have shown that certain stresses, in particular nutrient restriction, can positively impact on the life expectancy of cells. Even animals, such as mice, live longer when they eat less. The investigations carried out by Spang provide yet another building block in the more detailed understanding of the processes underlying an increase in lifespan. “It is also the P-body storage of mRNAs during sugar deficiency that proves to be of benefit to the lifespan of the cell,” says Spang.
(© Heike Sacher (University of Basel) / AcademiaNet)