Researchers at Stanford University have identified a new cellular pathway that clears misfolded proteins from the nucleus, which could have implications for therapies targeting age-related diseases like Alzheimer’s and Parkinson’s. Misfolded proteins can disrupt cellular functions and are linked to neurodegenerative conditions. The study, published in Nature Cell Biology, reveals how this clearing process involves communication between the nucleus and the cytoplasm, relying on a specific class of proteins that form vesicles for transporting molecules.
The team, led by Judith Frydman, utilized a combination of genetic, imaging, and biochemical techniques on yeast cells to track misfolded proteins. They discovered that these proteins generate inclusions resembling garbage dumps, which migrate to a junction between the nucleus and the vacuole—an organelle that degrades proteins. The research found that inclusions from both compartments work together to facilitate clearance.
Notably, the mechanism for delivering proteins from the nucleus to the vacuole differed from that of cytoplasmic proteins, indicating distinct yet coordinated protein management strategies within the cell. Future investigations will examine whether this pathway operates in mammalian cells and how aging impacts its efficiency.
