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In our team, we investigate effector proteins produced by Pseudomonas aeruginosa that contribute to its pathogenicity and niche colonization. By deciphering the pathogenic mechanisms involving these effectors, we aim to identify novel targets that could pave the way for anti-virulence strategies as an alternative to traditional antibiotic treatments against P. aeruginosa. One of our research focuses is the Tat (Twin-arginine translocation) pathway, which is responsible for exporting fully folded proteins across the inner membrane. In the first part of this seminar, I will discuss the critical role of the Tat system in P. aeruginosa physiology. I will present how a combination of in silico, proteomic, and genetic approaches allowed us to identify 34 substrate proteins that are exported via the Tat pathway. In the second part, I will explore the molecular mechanisms through which the Tat system contributes to copper resistance. I will show how we demonstrated that Tat mediates this resistance via two distinct mechanisms, operating in separate cellular compartments and responsive to different copper concentrations, highlighting a spatially and dose-dependent regulatory strategy
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