{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:17:33Z","timestamp":1791299853038,"version":"4.1.0"},"reference-count":30,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2008,2,1]],"date-time":"2008-02-01T00:00:00Z","timestamp":1201824000000},"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":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2008,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            We previously reported that deficiency of the\n            <jats:italic>lytH<\/jats:italic>\n            gene, whose product is homologous to lytic enzymes, caused the elevation of methicillin resistance in\n            <jats:italic>Staphylococcus aureus<\/jats:italic>\n            strain SR17238, a strain of\n            <jats:italic>S. aureus<\/jats:italic>\n            with a low level of resistance to methicillin (low-level MRSA) (J. Bacteriol. 179:6294-6301, 1997). In this study, we demonstrated that deficiency of\n            <jats:italic>lytH<\/jats:italic>\n            caused the same phenomenon in four other clinical isolates of low-level MRSA, suggesting this deficiency to exist in clinical isolates. We therefore searched the region including\n            <jats:italic>lytH<\/jats:italic>\n            in 127 clinical isolates of MRSA by PCR and found one strain, SR17164 (methicillin MIC, 1,600 \u03bcg\/ml), in which the\n            <jats:italic>lytH<\/jats:italic>\n            gene was inactivated by insertion sequence IS\n            <jats:italic>1182. lytH<\/jats:italic>\n            ::IS\n            <jats:italic>1182<\/jats:italic>\n            was replaced with intact\n            <jats:italic>lytH<\/jats:italic>\n            in this strain by integration and excision of the plasmid carrying the\n            <jats:italic>lytH<\/jats:italic>\n            region. Recombinants with intact\n            <jats:italic>lytH<\/jats:italic>\n            genes showed methicillin MICs of 800 \u03bcg\/ml, twofold lower than those of the recombinants with\n            <jats:italic>lytH<\/jats:italic>\n            ::IS\n            <jats:italic>1182<\/jats:italic>\n            and the parent. In addition,\n            <jats:italic>S. aureus<\/jats:italic>\n            SR17164, which has a high level of methicillin resistance, had properties similar to those caused by\n            <jats:italic>lytH<\/jats:italic>\n            deficiency; that is, the resistance levels of strain SR17164 and\n            <jats:italic>lytH<\/jats:italic>\n            -deficient variants from strain SR17238 were not significantly affected by\n            <jats:italic>llm<\/jats:italic>\n            inactivation, which greatly lowered resistance levels in most other high-level MRSA strains. These findings suggest that\n            <jats:italic>lytH<\/jats:italic>\n            inactivation contributed, to some extent, to the resistance level of\n            <jats:italic>S. aureus<\/jats:italic>\n            SR17164. To the best of our knowledge, this strain is the first clinical isolate of MRSA for which the genetic base for high-level resistance has been clarified.\n          <\/jats:p>","DOI":"10.1128\/aac.00395-07","type":"journal-article","created":{"date-parts":[[2007,12,11]],"date-time":"2007-12-11T01:44:26Z","timestamp":1197337466000},"page":"643-647","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["<i>Staphylococcus aureus<\/i>\n            Clinical Isolate with High-Level Methicillin Resistance with an\n            <i>lytH<\/i>\n            Mutation Caused by IS\n            <i>1182<\/i>\n            Insertion"],"prefix":"10.1128","volume":"52","author":[{"given":"Takaji","family":"Fujimura","sequence":"first","affiliation":[{"name":"Discovery Research Laboratories, Shionogi &amp; Co., Ltd., Toyonaka, Osaka 561-0825, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kazuhisa","family":"Murakami","sequence":"additional","affiliation":[{"name":"Discovery Research Laboratories, Shionogi &amp; Co., Ltd., Toyonaka, Osaka 561-0825, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0378-1119(87)90271-X"},{"key":"e_1_3_1_3_2","doi-asserted-by":"crossref","first-page":"93","DOI":"10.1111\/j.1574-6968.1999.tb13718.x","volume":"177","year":"1999","unstructured":"Chesneau, O., R. Lailler, A. Derbise, and N. E. Solh. 1999. Transposition of IS1181 in the genomes of Staphylococcus and Listeria. FEMS Microbiol. Lett.177:93-100.","journal-title":"FEMS Microbiol. Lett."},{"key":"e_1_3_1_4_2","doi-asserted-by":"crossref","first-page":"251","DOI":"10.1006\/plas.1994.1027","volume":"31","year":"1994","unstructured":"Derbise, A., K. G. H. Dyke, and N. E. Solh. 1994. Isolation and characterization of IS1181, an insertion sequence from Staphylococcus aureus. Plasmid31:251-264.","journal-title":"Plasmid"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1006\/plas.1996.0020"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0147-619X(92)90055-F"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/jb.179.20.6294-6301.1997"},{"key":"e_1_3_1_8_2","first-page":"109","year":"1989","unstructured":"Galas, D. J., and M. Chandler. 1989. Bacterial insertion sequences, p. 109-162. In D. E. Berg and M. M. Howe (ed.), Mobile DNA. 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