Effector-Effector Interplay and Coxiella Pathogenesis

3 Minute read

The goal of this project is to:

1. Use a systems-based approach to define physical interactions between important effector proteins.
2. Determine the role these interactions play during infection.
3. Use cell biology and biochemical approaches to decipher the function of interacting effectors.

The details

The bacterium responsible for Q fever, Coxiella burnetii, causes disease by multiplying inside human cells. Coxiella burnetii does this in a very innovative manner. It creates a vacuole, a membrane-bound compartment inside the cell, where it can safely replicate itself. To aid this process, the bacterium injects virulence proteins called effectors into the host to control its functions. To date, around 150 of these effectors have been identified. Despite this, we understand very little about how they function individually, and collectively, during infection. The traditional understanding of bacterial effector proteins is that they act on host targets. However, there is increasing evidence that shows that some effectors influence infection by acting on other effectors. This is an unexplored yet integral component of understanding host-pathogen interactions.

This project will:

• Use a systems-based approach to define physical interactions between important effector proteins
• Determine the role these interactions play during infection
• Use cell biology and biochemical approaches to decipher the function of interacting effectors.

This research will shed light on Coxiella pathogenesis and the complex cross-talk between the large cohort of effector proteins.

Supervision team

The University of Melbourne: Dr Hayley Newton

The University of Toronto: A/Prof Alexander Ensminger