{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T05:04:00Z","timestamp":1791263040982,"version":"4.1.0"},"reference-count":31,"publisher":"American Society for Microbiology","issue":"22","license":[{"start":{"date-parts":[[2003,11,15]],"date-time":"2003-11-15T00:00:00Z","timestamp":1068854400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2003,11,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The group B streptococcus (GBS) is an important human pathogen that infects newborns as well as adults. GBS also provides a model system for studying adaptation to different host environments due to its ability to survive in a variety of sites within the host. In this study, we have characterized a transcription factor, MtaR, that is essential for the ability of GBS to survive in vivo. An isogenic strain bearing a kanamycin insertion in\n            <jats:italic>mtaR<\/jats:italic>\n            was attenuated for survival in a neonatal-rat model of sepsis. The\n            <jats:italic>mtaR<\/jats:italic>\n            mutant grew poorly in human plasma, suggesting that its utilization of plasma-derived nutrients was inefficient. When an excess of exogenous methionine (200 \u03bcg\/ml) was provided to the\n            <jats:italic>mtaR<\/jats:italic>\n            mutant, its growth rate in plasma was restored to that of the wild-type strain. The\n            <jats:italic>mtaR<\/jats:italic>\n            mutant grew poorly in chemically defined medium (CDM) prepared with methionine at a concentration similar to that of plasma (4 \u03bcg\/ml) but was able to grow normally in CDM prepared with a high concentration of methionine (400 \u03bcg\/ml). Both the wild-type strain and the\n            <jats:italic>mtaR<\/jats:italic>\n            mutant were incapable of growth in CDM lacking methionine, indicating that GBS cannot synthesize methionine de novo. When the abilities of the strains to incorporate radiolabeled methionine were compared, the\n            <jats:italic>mtaR<\/jats:italic>\n            mutant incorporated fivefold less methionine than the wild-type strain during a 10-min period. Collectively, the results from this study suggest that the ability to regulate expression of a methionine transport system is critical for GBS survival in vivo.\n          <\/jats:p>","DOI":"10.1128\/jb.185.22.6592-6599.2003","type":"journal-article","created":{"date-parts":[[2003,11,2]],"date-time":"2003-11-02T18:12:22Z","timestamp":1067796742000},"page":"6592-6599","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":58,"title":["MtaR, a Regulator of Methionine Transport, Is Critical for Survival of Group B Streptococcus In Vivo"],"prefix":"10.1128","volume":"185","author":[{"given":"Daniel","family":"Shelver","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Childrens' Hospital and Regional Medical Center and University of Washington, Seattle, Washington 91805"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lakshmi","family":"Rajagopal","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Childrens' Hospital and Regional Medical Center and University of Washington, Seattle, Washington 91805"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa O.","family":"Harris","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Childrens' Hospital and Regional Medical Center and University of Washington, Seattle, Washington 91805"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig E.","family":"Rubens","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Infectious Disease, Childrens' Hospital and Regional Medical Center and University of Washington, Seattle, Washington 91805"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(05)80360-2"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.182.16.4466-4477.2000"},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"86","DOI":"10.1046\/j.1365-2567.1998.00402.x","volume":"93","year":"1998","unstructured":"Cornacchione, P., L. 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