Abstract

Aging is a common factor in many diseases, from diabetes to neurodegenerative disorders, and understanding the process of aging is crucial for preventing these illnesses.
In our bodies, proteins are the building blocks of cells, each possessing a specific role. However, as we age, some of these proteins become worn out and dysfunctional. This is where autophagy, a cellular process of “self-digestion,” comes into play. During autophagy, our old and damaged proteins are broken down into reusable components. But as we get older, this recycling process becomes less efficient, making our bodies more susceptible to age-related diseases.
My project focuses on ATG16, a protein found in all of our cells. It has a unique function of “tagging” cellular structures for recycling. Recently, it has been discovered that ATG16 can also tag vesicles that are destined to be transported outside the cell. My hypothesis is that this new role of ATG16 in mediating the secretion of cellular materials plays a significant role in the aging process. I employ model systems, such as the nematode C. elegans and mammalian cell cultures to understand how ATG16’s “tagging” process affects aging-related phenotypes.
The potential impact of my research is substantial, as it may uncover new roles for ATG16 in cellular processes and aging. Moreover, these findings may be instrumental in designing innovative drugs and new diagnostic tools that can target ATG16’s new functions. Such tools could help assess the risk as well as treat aging-related diseases.