The exocyst complex is an eight-subunit protein complex that assists in vesicle trafficking, specifically in the tethering of vesicles to the plasma membrane. Vesicle trafficking is critical to the exocytosis pathway, and cell polarity, which is responsible for guiding the cell to grow and develop properly. Mutations in the exocyst complex have been observed in humans and have been correlated with various diseases, from neurological disorders to early developmental disorders and more. This project investigates the previously identified human mutations in the exocyst complex and a conserved mutation, the loss of amino acids 429-461 in EXOC3 that cause an increase in HDL cholesterol, that is modelled in S. cerevisiae. Through cloning and the plasmid swap strategy, the mutant yeast strain demonstrated that the deleted residues were essential for the yeast to survive. Modelling mutations in yeast will help gain a more complete understanding of the structure and function of the exocyst complex and could assist in elucidating how the mutation affects human cell function and disease.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Jette, Brittany K.

Publisher

• Worcester Polytechnic Institute

Identifier

• 22711
• E-project-050621-091814

Palabra Clave

• HDL
• Sec6
• exocyst complex
• deletion
• human disease
• mutation

Advisor

• Vidali, Luis

Year

• 2021

Sponsor

• University of Massachusetts Medical School

Date created

• 2021-05-06

Resource type

• Major Qualifying Project

Major

• Biology & Biotechnology

Rights statement

• In Copyright