A single mechanosensitive channel protects Francisella tularensis subsp. holarctica from hypoosmotic shock and promotes survival in the aquatic environment

Francisella tularensis subsp. holarctica is found in North America and much of Europe and causes the disease tularemia in humans and animals. An aquatic cycle has been described for this subspecies, which has caused waterborne outbreaks of tularemia in at least 10 countries. In this study, we sought to identify the mechanosensitive channel(s) required for the bacterium to survive the transition from mammalian hosts to freshwater, which is likely essential for the transmission of the bacterium between susceptible hosts. A single 165-amino-acid MscS-type mechanosensitive channel (FtMscS) was found to protect F. tularensis subsp. holarctica from hypoosmotic shock, despite lacking much of the cytoplasmic vestibule domain found in well-characterized MscS proteins from other organisms. The deletion of this channel did not affect virulence within the mammalian host; however, FtMscS was required to survive the transition from the host niche to freshwater. The deletion of FtMscS did not alter the sensitivity of F. tularensis subsp. holarctica to detergents, H₂O₂, or antibiotics, suggesting that the role of FtMscS is specific to protection from hypoosmotic shock. The deletion of FtMscS also led to a reduced average cell size without altering gross cell morphology. The mechanosensitive channel identified and characterized in this study likely contributes to the transmission of tularemia between hosts by allowing the bacterium to survive the transition from mammalian hosts to freshwater.