The <i>Brucella</i> effector BspL targets the ER-associated degradation (ERAD) pathway and delays bacterial egress from infected cells
Jean‐Baptiste Luizet, Julie Raymond, Thaís Lourdes Santos Lacerda, Emeline Barbieux, Stanimir Kambarev, Magali Bonici, Frédérique Lembo, Kévin Willemart, Jean‐Paul Borg, Jean Celli, Francine C. A. Gérard, Éric Muraille, Jean‐Pierre Gorvel, Suzana P. Salcedo
Abstract
Significance Intracellular bacterial pathogens rely on dedicated systems to inject effector proteins into host cells and cause disease. This is the case for Brucella abortus , which causes brucellosis, one of the world’s most prevalent zoonotic diseases. We have found one such effector that can control the intracellular fate of Brucella by hijacking the machinery of the endoplasmic reticulum generally used by our cells to degrade misfolded or unwanted proteins. This bacterial effector works to slow down the formation of a specialized vacuole that enables Brucella to exit from the cell and infect neighboring cells. This delay ultimately allows the bacteria extra time for extensive intracellular multiplication, an essential feature of its virulence.