A tug of war: how Salmonella tackles cellular defense mechanisms
July 2019. Bacterial pathogens present a major public health concern, especially given the increasing emergence of antibiotic-resistant strains. As such, understanding the molecular details governing bacterial infection is of prime importance. A group of researchers from the Dikic group at Goethe University and the group of Danielle Malo at McGill University (Canada) recently joined forces and this month published a first collaborative article in the journal Nature Microbiology. Their study focuses on non-typhoidal Salmonella infections caused by Salmonella Typhimurium, a food-borne bacterial pathogen that infects the intestinal tract.
The study was mainly motivated by the clinical implications of these infections, with non-typhoidal Salmonella accounting for approximately 93.8 million illnesses and 155,000 deaths worldwide per year. Through adopting a multi-disciplinary approach, the researchers were able to uncover an important host protein, which they named CYRI. This protein is implicated in combating Salmonella infections. The team revealed how Salmonella fights back by reducing the levels of this protein upon infection. Interestingly, the scientists also found a protective role for CYRI in infections mediated by Mycobacterium tuberculosis and Listeria monocytogenes. This demonstrates that CYRI drives important signalling events that are relevant in the context of infections by different intracellular bacterial pathogens.
Kyoko E. Yuki, Hadir Marei, Evgenij Fiskin, Megan M. Eva, Angelica A. Gopal, Jeremy A. Schwartzentruber, Jacek Majewski, Mathieu Cellier, Judith N. Mandl, Silvia M. Vidal, Danielle Malo* & Ivan Dikic* (2019) CYRI/FAM49B negatively regulates RAC1-driven cytoskeletal remodelling and protects against bacterial infection. Nature Microbiology: published online 8 July 2019.
Ivan Dikic, Buchmann Institute for Molecular Life Sciences and Institute of Biochemistry II, Goethe University Frankfurt, Frankfurt/Main, Germany, dikic(at)biochem2.uni-frankfurt.de.