A manganese-sparing response balances competing cellular demands to enable <i>Staphylococcus aureus</i> infection

During infection, pathogens must utilize processes that impose conflicting cellular demands. This conflict is exemplified by the need of <i>Staphylococcus aureus</i> to preserve essential processes and survive the oxidative burst of immune cells, both of which require manganese despite experiencing host-imposed manganese starvation. The current investigations revealed that <i>S. aureus</i> activates a manganese-sparing response controlled by the regulatory RNA, RsaC, in response to host-imposed manganese starvation. This small RNA sacrifices the expression of a manganese-dependent superoxide dismutase to preserve the activity of essential manganese-dependent processes. Despite this, RsaC is necessary for infection, revealing the important role of this manganese-sparing response to pathogenesis and that invaders must actively compromise ideal stress responses to cause disease.