Researchers led by Zachery R. Belak and Troy A.A. Harkness from the University of Saskatchewan and the University of Alberta published a study on Apr. 3 showing how yeast cells can be used to model premature aging caused by Progerin, according to a paper in Volume 18 of Aging-US.
The research matters because Hutchinson–Gilford Progeria Syndrome is a rare disorder linked to early onset aging, and understanding its cellular mechanisms could lead to new approaches for improving health during aging.
In their work, the team genetically engineered yeast cells to express Progerin—the toxic protein responsible for progeria—and compared its effects with those of Lamin A, its normal counterpart. The researchers found that Progerin expression slowed cell growth, increased genome instability, and reduced chronological lifespan in yeast cells. Lamin A did not produce these harmful effects.
The study also showed that Progerin accumulates in older mother cells and is more stable than Lamin A. This suggests that damaged or toxic proteins may be retained as cells age—a process similar to what has been seen in human cells.
"Taken together, expression of Progerin in yeast cells mimics what is observed in human cells, establishing yeast as a powerful model to discover genetic mechanisms driving premature and normal aging," said the authors.
The findings present an efficient way for scientists to explore how toxic proteins affect cellular health during aging and offer a platform for testing new strategies aimed at reducing such protein accumulation.
