PhoU homologs from dimerization and protein interactions.

PhoU proteins are negative regulators of the phosphate response, regulate virulence, and contribute to antibiotic resistance. has multiple genes encoding PhoU homologs that regulate persister formation and potentially virulence, but the molecular mechanisms of this regulation are not fully understood. We used a bacterial adenylate cyclase two-hybrid system to assess interactions between PhoU homologs and other proteins known to interact with PhoU from PhoU (also referred to as PhoU1) interacted with PhoU itself; PitR (also referred to as PhoU2) interacted with PitR itself.

Human Serum Alters the Metabolism and Antibiotic Susceptibility of .

is a common source of hospital-acquired bacterial infections, where the emergence of antibiotic resistance is a serious human health concern. Most investigations into virulence and antibiotic resistance have relied on cultivation conditions and optimized media formulations. However, can survive and adapt to a hostile host environment or antibiotic treatments by rapidly adjusting its metabolic activity.

Metabolic changes associated with adaptive resistance to daptomycin in Streptococcus mitis-oralis.

Background: Viridans group streptococci of the Streptococcus mitis-oralis subgroup are important endovascular pathogens. They can rapidly develop high-level and durable non-susceptibility to daptomycin both in vitro and in vivo upon exposure to daptomycin. Two consistent genetic adaptations associated with this phenotype (i.

Control of the Regulon in .

Phosphorus is required for many biological molecules and essential functions, including DNA replication, transcription of RNA, protein translation, posttranslational modifications, and numerous facets of metabolism. In order to maintain the proper level of phosphate for these processes, many bacteria adapt to changes in environmental phosphate levels. The mechanisms for sensing phosphate levels and adapting to changes have been extensively studied for multiple organisms.

Metabolic interventions for the prevention and treatment of daptomycin non-susceptibility in Staphylococcus aureus.

Background: A major developing problem in the treatment of Staphylococcus aureus infections is the emergence of resistance during treatment with daptomycin. Previous metabolomic analyses of isogenic S. aureus strains prior to and after evolution into a daptomycin non-susceptible (DapNS) state provided important metabolic information about this transition (e.

Genetic analysis, structural modeling, and direct coupling analysis suggest a mechanism for phosphate signaling in Escherichia coli.

Background: Proper phosphate signaling is essential for robust growth of Escherichia coli and many other bacteria. The phosphate signal is mediated by a classic two component signal system composed of PhoR and PhoB. The PhoR histidine kinase is responsible for phosphorylating/dephosphorylating the response regulator, PhoB, which controls the expression of genes that aid growth in low phosphate conditions.

The PhoU protein from Escherichia coli interacts with PhoR, PstB, and metals to form a phosphate-signaling complex at the membrane.

Robust growth in many bacteria is dependent upon proper regulation of the adaptive response to phosphate (Pi) limitation. This response enables cells to acquire Pi with high affinity and utilize alternate phosphorous sources. The molecular mechanisms of Pi signal transduction are not completely understood.