FIG 8.

Hypothetical model for the antibacterial mode of action of GA (15:1) against Gram-positive pathogens by cross talk with iron homeostasis. When GA (15:1) is present, it destabilizes the iron homeostasis and creates a state of iron starvation, which triggers the iron starvation response: Fur-mediated repression of iron uptake transporters is relieved, and iron transporters are upregulated, allowing Fe³⁺ to enter the bacterial cells. In addition, GA (15:1) blocks protein biosynthesis and inhibits the growth and cell division of the bacterium through unidentified targets. Meanwhile, the iron starvation condition can strengthen this process.