SCAN:"Legionella pneumophila effector VipA: an actin nucleator that interferes with host cell organelle trafficking"

ITQB-SCAN Seminar

Title:Legionella pneumophila effector VipA: an actin nucleator that interferes with host cell organelle trafficking

Speaker: Irina Franco

From: Infection Biology Laboratory

Abstract:

Legionella pneumophila is a facultative intracellular bacterium that can cause a frequently fatal type of pneumonia known as Legionnaires' disease. In nature, L. pneumophila is found in both fresh water and soil where it parasitizes free-living protists. Upon inhalation of contaminated aerosols, L. pneumophila invades and replicates in human alveolar macrophages, leading to inflammation and development of the disease. In both macrophages and protozoan cells the bacteria resides and replicates inside a modified phagosome, the Legionella-containing vacuole (LCV).
Legionella uses a Type IVB Secretion System to translocate a multitude of “effector” proteins into the host cell that modify eukaryotic vesicle trafficking pathways and prevent fusion of the newly formed phagosome with the lysosome, thus avoiding degradation. One of these effectors is VipA, a protein that binds actin in vitro and nucleates its polymerization without the requirement of additional host factors. During infection of macrophages, secreted VipA localizes in puncta that colocalize with actin-rich regions and early endosomes. When ectopically expressed in S. cerevisiae VipA interferes with the Multivesicular Body (MVB) pathway and associates with some of its components, as well as with actin filaments, and the ability to disrupt the MVB pathway is associated with the capacity to bind actin. These results are consistent with a model where VipA, through its dual function of regulating actin dynamics and binding to endosomal organelles, may play a role in altering vesicle trafficking in order to enable the pathogen to escape degradation.