Vibrio parahaemolyticus, a Gram‐negative bacterium, is the leading cause of seafood‐borne illness in the United States. This pathogen is able to infect and survive in humans by manipulating the host cellular machinery via bacterial Type III effector proteins that are translocated into the host cell, where they disrupt cellular signaling. One of the principal effector proteins, VopQ, has been demonstrated to be necessary and sufficient to induce autophagosome accumulation. I propose to elucidate the precise cellular and molecular mechanism by which VopQ induces autophagosome accumulation. Since autophagosomes are transient vesicles, the accumulation could be due to an increase in formation of autophagosomes or a decrease in lysosomal fusion. Using biochemical assays and yeast genetics we have uncovered a novel target that reveals the role of VopQ in vesicle fusion during autophagy.With the discovery of several bacterial effectors that function to manipulate host membranes, many eukaryotic vesicle trafficking pathways have been unveiled, and many new questions have surfaced about the mechanisms of novel bacterial effectors. Understanding the mechanism by which VopQ induces autophagosome accumulation could be essential in understanding V. para infection and could give new insights into the mechanisms of eukaryotic vesicle trafficking.