A deadly bacterial toxin is not just leaked when the cell dies, but is actively controlled by how sticky the bacteria's surface is.
Streptococcus pneumoniae releases a toxin called pneumolysin that causes severe lung damage in patients. Scientists previously thought this toxin was only released as a byproduct when the bacterial cells eventually burst and died. This study shows that the bacteria actually regulate the toxin's release through the physical hydrophobicity, or stickiness, of their own cell walls. By managing the production of lipoteichoic acids, the bacteria can choose when to unleash their chemical weapons. Targeting this specific surface-sticking mechanism could provide a new way to neutralize the bacteria without needing to kill them with antibiotics.
TacL-dependent Lipoteichoic Acid Biosynthesis Regulates Pneumolysin Release in Streptococcus pneumoniae
SSRN · 6718768
Streptococcus pneumoniae regulates its virulence by controlling the release of pneumolysin (Ply), a critical pore-forming toxin whose release is governed by the cell wall. Although lipoteichoic acids (LTAs) are major cell wall components in Gram-positive bacteria, their function in modulating Ply release remains unclear. Traditional studies have suggested that Ply is mainly released through cell wall damage-triggered autolysis. Here we show that TacL-mediated LTA biosynthesis is essential for co