NEW DELHI, India — Researchers at the Jawaharlal Nehru Centre for Advanced Scientific Research have identified a previously unrecognized cellular mechanism involved in autophagy, a discovery that could help advance treatments for neurodegenerative diseases such as Alzheimer’s and Parkinson’s, as well as certain cancers.
Autophagy, often described as the cell’s “self-eating” process, allows cells to remove damaged or unnecessary components and maintain internal balance. When this process breaks down, especially in long-lived cells like neurons, cellular waste accumulates, contributing to diseases including Alzheimer’s and Huntington’s.
In cancer, autophagy plays a complex, dual role. It can suppress tumor formation by maintaining genome integrity and clearing damaged proteins and mitochondria, but in later stages some cancer cells exploit autophagy to support their survival and growth. Understanding how autophagy is regulated is therefore critical for developing effective therapies.
The JNCASR team, an autonomous institution under the Department of Science and Technology, discovered that the exocyst complex — a group of proteins traditionally known for transporting molecules to the cell surface — also plays a crucial role in autophagy.
The exocyst complex consists of eight proteins. The researchers found that seven of these eight proteins are required for the formation of autophagosomes, the membrane-bound structures that act as cellular “trash bags” to enclose and remove waste. When the complex is absent or dysfunctional, autophagosome formation is impaired, leading to defective cellular cleanup machinery.
Led by Prof. Ravi Manjithaya, the team used yeast cells as a model system to study how autophagosomes form, providing insights applicable to more complex organisms. Their work revealed how the exocyst complex, previously associated mainly with secretion, also contributes directly to the autophagy pathway.
Because defects in autophagy are linked to a wide range of neurodegenerative diseases and cancers, the findings could open new strategies for regulating this pathway and restoring cellular balance.
The study was published in the journal Proceedings of the National Academy of Sciences and is expected to spur further research into therapeutic approaches that target autophagy-related mechanisms. (Source: IANS)
