In work published in Infection and Immunity, graduate student Jessica Kelliher, from the laboratory of Dr. Thomas Kehl-Fie, investigated how the superbug Staphylococcus aureus regulates the acquisition of phosphate.

The study revealed that S. aureus uses a highly conserved regulator, PhoPR, to coordinate phosphate uptake and respond to phosphate availability.

At the same time, they also revealed that S. aureus possesses an expanded repertoire of accessory regulatory proteins, suggesting that the staphylococcal phosphate regulatory circuit differs from that found in other bacteria.

Consistent with a role in phosphate homeostasis, PhoPR induced the expression of phosphate importers in phosphate-limited environments. Surprisingly, these investigations also revealed that in some phosphate-limited environments, the contribution of PhoPR to growth was independent of its role in regulating phosphate transporter expression.

Similarly, during infection, the subset of genes controlled by PhoPR that contributed to the ability of S. aureus to cause disease was dependent on the site of infection. Cumulatively, these findings point to an important role for PhoPR in orchestrating phosphate acquisition, as well as transporter-independent mechanisms, that contribute to S. aureus virulence.