Progerin Expression Creates a Yeast Model of Premature Aging

Aging is shaped not only by changes in DNA and metabolism but also by the gradual accumulation of proteins that cells struggle to remove. One striking example is Progerin, an abnormal form of lamin A that accumulates at the nuclear periphery in Hutchinson-Gilford Progeria Syndrome, or HGPS. A new study shows that expressing this human protein in budding yeast reproduces several aging-related cellular defects and creates a simple experimental system for studying how toxic proteins accumulate and affect lifespan.
A research paper published in Volume 18 of Aging titled “Modeling premature aging in yeast via the expression of Progerin,” developed a yeast model in which human Progerin and its normal counterpart, lamin A, were expressed as fluorescent fusion proteins.
The study was led by first author Zachery R. Belak of the University of Saskatchewan, with corresponding author Troy AA. Harkness, affiliated with the University of Saskatchewan and the University of Alberta.
The researchers found that Progerin localized to the yeast nuclear membrane, slowed cellular growth, shortened chronological lifespan, increased genomic instability, and was preferentially retained in older mother cells. Together, these findings suggest that yeast can reproduce several cellular consequences associated with Progerin accumulation despite lacking the conventional nuclear lamina found in human cells.
Full blog post - https://aging-us.org/2026/10/progerin-expression-creates-a-yeast-model-of-premature-aging/
DOI - https://doi.org/10.18632/aging.206367
Corresponding author - Troy AA. Harkness - taharkne@ualberta.ca
Abstract video - https://www.youtube.com/watch?v=VYQKAJjgIb8
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Keywords - aging, Hutchinson-Gilford Progeria Syndrome, yeast, Progerin, Lamin A, premature aging
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