{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Parraga Solorzano PK"],"funding":["NIAID NIH HHS","Vallee Foundation","HHS | NIH | National Institute of Allergy and Infectious Diseases","HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)"],"pagination":["e0322322"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9973326"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["The preferred carbon source of Staphylococcus aureus and many other pathogens is glucose, and its consumption is critical during infection. However, glucose utilization increases the cellular demand for manganese, a nutrient sequestered by the host as a defense against invading pathogens. Therefore, bacteria must balance glucose metabolism with the increasing demand that metal-dependent processes, such as glycolysis, impose upon the cell. A critical regulator that enables S. aureus to resist nutritional immunity is the ArlRS two-component system. This work revealed that ArlRS regulates the expression of FdaB, a metal-independent fructose 1,6-bisphosphate aldolase. Further investigation revealed that when S. aureus is metal-starved by the host, FdaB functionally replaces the metal-dependent"],"journal":["mBio"],"pubmed_title":["A Manganese-independent Aldolase Enables Staphylococcus aureus To Resist Host-imposed Metal Starvation."],"pmcid":["PMC9973326"],"funding_grant_id":["R21 AI149115","R01 AI 118880","R01 AI155611","R21 AI 149115","R01 AI 155611","R01 AI118880"],"pubmed_authors":["Radin JN","Parraga Solorzano PK","Bastille TS","Kehl-Fie TE"],"additional_accession":[]},"is_claimable":false,"name":"A Manganese-independent Aldolase Enables Staphylococcus aureus To Resist Host-imposed Metal Starvation.","description":"The preferred carbon source of Staphylococcus aureus and many other pathogens is glucose, and its consumption is critical during infection. However, glucose utilization increases the cellular demand for manganese, a nutrient sequestered by the host as a defense against invading pathogens. Therefore, bacteria must balance glucose metabolism with the increasing demand that metal-dependent processes, such as glycolysis, impose upon the cell. A critical regulator that enables S. aureus to resist nutritional immunity is the ArlRS two-component system. This work revealed that ArlRS regulates the expression of FdaB, a metal-independent fructose 1,6-bisphosphate aldolase. Further investigation revealed that when S. aureus is metal-starved by the host, FdaB functionally replaces the metal-dependent","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2026-06-14T03:23:25.851Z","creation":"2025-04-07T13:05:19.263Z"},"accession":"S-EPMC9973326","cross_references":{"pubmed":["36598285"],"doi":["10.1128/mbio.03223-22"]}}