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Elucidating the role of exocyst in autophagy and its implications in human diseases

Implementing Organization

Principal Investigator
Dr. Ravi Manjithaya
Jawaharlal Nehru Centre For Advanced Scientific Research, Karnataka

Project Overview

Autophagy is an intracellular degradative pathway that involves the formation of autophagosomes, which capture and deliver degraded cargo to the vacuole/lysosomes. This process maintains homeostasis within the cell by clearing unwanted material, including pathogens, and providing nutrients during starvation stress. The autophagy pathway is affected by complex diseases like neurodegeneration and cancer. Approximately 42 unique genes have been identified for this pathway, and genes involved in other pathways have also been identified. To identify key players in autophagy, a screen was conducted using yeast as a model system. Several genes of the exocyst complex were identified as hits from the screen. The exocyst complex is a multisubunit tethering complex that tethers vesicles to the plasma membrane. The role of exocyst in autophagy is unclear, but it is involved in autophagosome biogenesis. Further studies are being conducted to understand the contribution of the exocyst in the progression of autophagosome biogenesis stages, such as initiation, expansion, completion, maturation, and fusion with the vacuole. To identify disease-associated SNPs of the exocyst complex, both genetic and biochemical approaches will be utilized. This will contribute to our understanding of the role of exocyst in autophagosome biogenesis and shed light on the regulation and contribution of autophagy flux in health and disease.

Source

Source
Anusandhan National Research Foundation/Science and Engineering Research Board (SERB), DST 2023-24
Funding Organization
Quick Information
Area of Research
Life Sciences & Biotechnology
Start Date
2023
End Date
2026
Status
Ongoing
Contact
ravim@jncasr.ac.in
Output
No. of Research Paper
00
Technologies (If Any)
00
No. of PhD Produced
00
Publications
00
No. of Patents
Filed : 00
Grant : 00
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