The bacterium Bacillus anthracis — the cause of the serious infectious disease anthrax — has been used as a bioterror agent. Understanding how B. anthracis adapts to hostile environments to cause infection may identify new targets for treatment.
Eric Skaar, PhD, and colleagues studied the response of B. anthracis to targocil, an antimicrobial compound that damages the cell envelope.
They demonstrated that targocil treatment activates a “two-component system” called EdsRS, which increases the production of a membrane phospholipid (cardiolipin) through a previously uncharacterized cardiolipin synthase enzyme. Cardiolipin is then used to repair the envelope and maintain B. anthracis viability and fitness.
The findings, reported in the journal mBio, highlight the adaptability of B. anthracis and reveal a mechanism the pathogen uses to defend against structural damage and resist antimicrobial toxicity. The work underscores the importance of studying two-component systems like EdsRS that B. anthracis uses to adapt to its environment and cause disease.
This research was supported by the National Institutes of Health (grants AI073843, GM103391, ES007028), Grove City College Swezey Fund, Jewell, Moore, and MacKenzie Fund, and Ernest W. Goodpasture Professorship.