{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,16]],"date-time":"2026-04-16T07:02:30Z","timestamp":1776322950992,"version":"3.50.1"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2024,12,31]],"date-time":"2024-12-31T00:00:00Z","timestamp":1735603200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 AI139244"],"award-info":[{"award-number":["R01 AI139244"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,7,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Methicillin-resistant Staphylococcus aureus (MRSA) is a leading cause of endovascular infections. The prophage-encoded protein Gp05 has been identified as a critical virulence factor that contributes to MRSA persistence during vancomycin treatment in an experimental endocarditis model. However, the mechanisms underlying this persistence phenotype remain poorly understood.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>This study investigated the genetic factors contributing to Gp05-associated MRSA persistence utilizing RNA sequencing (RNA-seq) on an isogenic MRSA strain set, including a clinical persistent bacteremia isolate, its chromosomal gp05 deletion mutant, and gp05-complemented strains.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>RNA-seq revealed significant downregulation of the GraSR two-component regulatory system and its downstream genes, mprF and dltABCD, in the gp05 deletion mutant compared to the wild-type and gp05-complemented strains. This downregulation led to a substantial shift in membrane phospholipid composition, with an increased phosphatidylglycerol and a corresponding decrease in lysyl-phosphatidylglycerol. These changes resulted in increased susceptibility of the gp05 deletion mutant to human cationic antimicrobial peptide (CAMP) LL-37, neutrophils, and vancomycin. These results were confirmed in an isogenic gp05 overexpression strain set in MRSA JE2 background.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Gp05 modulates MRSA surface phospholipid components and charge, offering new insights into the molecular mechanisms underlying Gp05-mediated persistence in endovascular infections and potential therapeutic targets to combat these infections.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/infdis\/jiae640","type":"journal-article","created":{"date-parts":[[2024,12,31]],"date-time":"2024-12-31T07:46:53Z","timestamp":1735631213000},"page":"1512-1520","source":"Crossref","is-referenced-by-count":2,"title":["Phage-Encoded Virulence Factor, Gp05, Alters Membrane Phospholipids and Reduces Antimicrobial Susceptibility in Methicillin-Resistant <i>Staphylococcus aureus<\/i>"],"prefix":"10.1093","volume":"231","author":[{"given":"Yi","family":"Li","sequence":"first","affiliation":[{"name":"Lundquist Institute for Biomedical Innovation, Harbor-University of California, Los Angeles Medical Center , Torrance"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nagendra N","family":"Mishra","sequence":"additional","affiliation":[{"name":"Lundquist Institute for Biomedical Innovation, Harbor-University of California, Los Angeles Medical Center , Torrance"},{"name":"Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5845-2235","authenticated-orcid":false,"given":"Liang","family":"Chen","sequence":"additional","affiliation":[{"name":"School of Pharmacy and Pharmaceutical Sciences, University at Buffalo , New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adhar C","family":"Manna","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth , Hanover, New Hampshire"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ambrose L","family":"Cheung","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth , Hanover, New Hampshire"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard A","family":"Proctor","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Medical Microbiology\/Immunology, University of Wisconsin School of Medicine and Public Health , Madison"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan Q","family":"Xiong","sequence":"additional","affiliation":[{"name":"Lundquist Institute for Biomedical Innovation, Harbor-University of California, Los Angeles Medical Center , Torrance"},{"name":"Department of Medicine, David Geffen 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