Pseudomonas Rhamnolipids Induces Membrane Stress Response in Mycobacteria

Presenter

Alkmini Diamantidi

Campus

UMass Amherst

Sponsor

Yasu S. Morita, Department of Microbiology, UMass Amherst

Schedule

Session 4, 2:30 PM - 3:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A38, Campus Center Auditorium, Row 2 (A21-A40) [Poster Location Map]

Abstract

Tuberculosis (TB) is the second leading cause of death by infectious diseases. Approximately a quarter of the world’s population is believed to have contracted TB bacteria, and about 5-10% of those will eventually exhibit symptoms and progress to TB disease. TB is caused by the bacterium Mycobacterium tuberculosis and mostly affects the lungs. The key characteristic of mycobacteria is their double membrane cell envelope that is rich in lipids and carbohydrates. The complex cell envelope of mycobacteria provides multiple mechanisms for their survival and pathogenicity, making them challenging to treat with antibiotics. One critical part of the cell envelope is a lipid known as phosphatidylinositol mannosides (PIMs). The inositol acylation of monoacyl PIMs to diacyl PIMs as a response to membrane stress is a concept that is of great interest to us. A previous study has shown this membrane stress response happening upon treatment of the bacteria with certain membrane-fluidizing compounds. Rhamnolipids are naturally occurring biosurfactants, which are produced by various species of bacteria, particularly Pseudomonas aeruginosa. We considered the possibility that biosurfactants like rhamnolipids may induce PIM acylation. Here, we show that rhamnolipids cause PIM inositol acylation in Mycobacterium smegmatis. 

Keywords

stress response, mycobacteria, cell envelope

Research Area

Biological Organisms

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