In order to cause disease, the human pathogen Staphylococcus aureus must adapt to the changing host environment. Many of these adaptations are mediated through two-component signal transduction systems (TCSs) that coordinate gene expression in response to environmental stimuli. In a new study reported in the Journal of Bacteriology, researchers at Illinois provide insight into the signal transduction mechanism utilized by the staphylococcal TCS ArlRS in response to host-imposed manganese and glucose starvation.
“Signal transduction systems, such as ArlRS, play critical roles in allowing pathogens to adapt to the ever-changing environment that pathogens encounter during infection and thus are critical contributors to disease,” said Thomas Kehl-Fie (MMG), an associate professor of microbiology and leader of the study.
To limit S. aureus pathogenicity, the host sequesters essential nutrients—a process called nutritional immunity—such as manganese, zinc, and iron during infection. However, successful pathogens can circumvent this host defense and cause disease. The researchers zeroed in on one mechanism utilized by S. aureus to evade this host response that relies on the ArlRS two-component system, which comprises the histidine kinase ArlS and response regulator protein ArlR.
“We are particularly interested in elucidating how ArlR is activated, as this response regulator is implicated in the ability of S. aureus to both survive nutrient limitation and coordinate a response...
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