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Publications of the Week

The Redox-Responsive Transcriptional Regulator Rex Represses Fermentative Metabolism and Is Required for Listeria monocytogenes Pathogenesis

By August 20, 2021August 24th, 2021No Comments

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This week we profile a recent publication in PLOS Pathogens from the laboratory of Dr. Michelle Reniere at UW.

Can you provide a brief overview of your lab’s current research focus?

Research in the Reniere lab is aimed at understanding how bacterial pathogens recognize and adapt to their host. We utilize Listeria monocytogenes as a model organism to investigate how intracellular pathogens sense different environments within the host in order to activate their virulence and metabolic programs. Specifically, we are interested in defining the redox signaling pathways critical for L. monocytogenes pathogenesis.

What is the significance of the findings of this publication?

In this work, we characterized the role of the redox-responsive transcriptional regulator Rex in Listeria monocytogenes growth and pathogenesis. We demonstrated that alleviation of Rex repression coordinates expression of genes necessary in the GI tract during infection, including fermentative metabolism and virulence determinants. Furthermore, we determined that Rex-dependent regulation was required for bacterial replication in peripheral organs, specifically within the gallbladder. Overall, our results demonstrated that Rex-mediated redox sensing and transcriptional regulation are important for L. monocytogenes metabolic adaptation and virulence during infection.

What are the next steps for this research?

Within a host Listeria monocytogenes traffics through a multiorgan life cycle where it eventually colonizes the gallbladder, which becomes the primary reservoir of bacteria during infection. Ongoing work is aimed at defining the gallbladder as a replicative niche for bacterial pathogens. Furthermore, we are interested in identifying the factors required for L. monocytogenes survival and replication within the gallbladder.

If you’d like us to mention your funding sources, please list them.

NIH grants R01AI132356 and T32AI055396

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