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Inhibition of exotoxin production by mobile genetic element SCCmec-encoded psm-mec RNA is conserved in staphylococcal species
Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCCmec. We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. H...
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| Published in: | PloS one 2014-06, Vol.9 (6), p.e100260-e100260 |
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| creator | Ikuo, Mariko Nagano, Gentaro Saito, Yuki Mao, Han Sekimizu, Kazuhisa Kaito, Chikara |
| description | Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCCmec. We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. Here, we examined whether the regulatory role of psm-mec on host bacterial virulence properties is conserved among other staphylococcal species, S. epidermidis and S. haemolyticus, both of which are important causes of nosocomial infections. In S. epidermidis, introduction of psm-mec decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation. Introduction of psm-mec with a stop-codon mutation that did not express PSM-mec protein but did express psm-mec RNA also decreased PSM production, but did not increase biofilm formation. Thus, the psm-mec RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in S. epidermidis. In S. haemolyticus, introduction of psm-mec decreased PSM production, but did not affect biofilm formation. The mutated psm-mec with a stop-codon also caused the same effect. Thus, the psm-mec RNA also inhibits PSM production in S. haemolyticus. These findings suggest that the inhibitory role of psm-mec RNA on exotoxin production is conserved among staphylococcal species, although the stimulating effect of the psm-mec gene on biofilm formation is not conserved. |
| doi_str_mv | 10.1371/journal.pone.0100260 |
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We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. Here, we examined whether the regulatory role of psm-mec on host bacterial virulence properties is conserved among other staphylococcal species, S. epidermidis and S. haemolyticus, both of which are important causes of nosocomial infections. In S. epidermidis, introduction of psm-mec decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation. Introduction of psm-mec with a stop-codon mutation that did not express PSM-mec protein but did express psm-mec RNA also decreased PSM production, but did not increase biofilm formation. Thus, the psm-mec RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in S. epidermidis. In S. haemolyticus, introduction of psm-mec decreased PSM production, but did not affect biofilm formation. The mutated psm-mec with a stop-codon also caused the same effect. Thus, the psm-mec RNA also inhibits PSM production in S. haemolyticus. These findings suggest that the inhibitory role of psm-mec RNA on exotoxin production is conserved among staphylococcal species, although the stimulating effect of the psm-mec gene on biofilm formation is not conserved.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0100260</identifier><identifier>PMID: 24926994</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antibiotic resistance ; Antibiotics ; Bacteria ; Biofilms ; Biofilms - growth & development ; Biology and Life Sciences ; Conserved Sequence ; Drug resistance ; Exotoxins ; Exotoxins - genetics ; Gene Expression Regulation, Bacterial ; Gene Silencing - physiology ; Genes ; Genomes ; Gram-positive bacteria ; Health aspects ; Hospitals ; Interspersed Repetitive Sequences - physiology ; Laboratories ; Mec gene ; MEC protein ; Medicine and Health Sciences ; Mutation ; Neutrophils ; Nosocomial infection ; Pathogens ; Pharmaceutical sciences ; Phenols ; Phenotype ; Plasmids ; Proteins ; Ribonucleic acid ; RNA ; RNA, Bacterial - genetics ; Species ; Standard deviation ; Staphylococcus ; Staphylococcus - genetics ; Staphylococcus - growth & development ; Staphylococcus - pathogenicity ; Staphylococcus aureus ; Staphylococcus aureus - genetics ; Staphylococcus aureus - growth & development ; Staphylococcus epidermidis ; Staphylococcus epidermidis - genetics ; Staphylococcus epidermidis - growth & development ; Staphylococcus epidermidis - pathogenicity ; Staphylococcus haemolyticus - genetics ; Staphylococcus haemolyticus - growth & development ; Staphylococcus haemolyticus - pathogenicity ; Staphylococcus infections ; Toxins ; Transposons ; Virulence ; Virulence (Microbiology) ; Virulence - genetics ; Wildlife conservation</subject><ispartof>PloS one, 2014-06, Vol.9 (6), p.e100260-e100260</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Ikuo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Ikuo et al 2014 Ikuo et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c688t-e8fb43770f458c6572326ebc3435312b2196a694b9f65cf6d564ed1a1f323fa43</citedby><cites>FETCH-LOGICAL-c688t-e8fb43770f458c6572326ebc3435312b2196a694b9f65cf6d564ed1a1f323fa43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1978567260/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1978567260?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24926994$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Becker, Karsten</contributor><creatorcontrib>Ikuo, Mariko</creatorcontrib><creatorcontrib>Nagano, Gentaro</creatorcontrib><creatorcontrib>Saito, Yuki</creatorcontrib><creatorcontrib>Mao, Han</creatorcontrib><creatorcontrib>Sekimizu, Kazuhisa</creatorcontrib><creatorcontrib>Kaito, Chikara</creatorcontrib><title>Inhibition of exotoxin production by mobile genetic element SCCmec-encoded psm-mec RNA is conserved in staphylococcal species</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCCmec. We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. Here, we examined whether the regulatory role of psm-mec on host bacterial virulence properties is conserved among other staphylococcal species, S. epidermidis and S. haemolyticus, both of which are important causes of nosocomial infections. In S. epidermidis, introduction of psm-mec decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation. Introduction of psm-mec with a stop-codon mutation that did not express PSM-mec protein but did express psm-mec RNA also decreased PSM production, but did not increase biofilm formation. Thus, the psm-mec RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in S. epidermidis. In S. haemolyticus, introduction of psm-mec decreased PSM production, but did not affect biofilm formation. The mutated psm-mec with a stop-codon also caused the same effect. Thus, the psm-mec RNA also inhibits PSM production in S. haemolyticus. 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genetics</subject><subject>Species</subject><subject>Standard deviation</subject><subject>Staphylococcus</subject><subject>Staphylococcus - genetics</subject><subject>Staphylococcus - growth & development</subject><subject>Staphylococcus - pathogenicity</subject><subject>Staphylococcus aureus</subject><subject>Staphylococcus aureus - genetics</subject><subject>Staphylococcus aureus - growth & development</subject><subject>Staphylococcus epidermidis</subject><subject>Staphylococcus epidermidis - genetics</subject><subject>Staphylococcus epidermidis - growth & development</subject><subject>Staphylococcus epidermidis - pathogenicity</subject><subject>Staphylococcus haemolyticus - genetics</subject><subject>Staphylococcus haemolyticus - growth & development</subject><subject>Staphylococcus haemolyticus - pathogenicity</subject><subject>Staphylococcus infections</subject><subject>Toxins</subject><subject>Transposons</subject><subject>Virulence</subject><subject>Virulence (Microbiology)</subject><subject>Virulence - 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growth & development</topic><topic>Biology and Life Sciences</topic><topic>Conserved Sequence</topic><topic>Drug resistance</topic><topic>Exotoxins</topic><topic>Exotoxins - genetics</topic><topic>Gene Expression Regulation, Bacterial</topic><topic>Gene Silencing - physiology</topic><topic>Genes</topic><topic>Genomes</topic><topic>Gram-positive bacteria</topic><topic>Health aspects</topic><topic>Hospitals</topic><topic>Interspersed Repetitive Sequences - physiology</topic><topic>Laboratories</topic><topic>Mec gene</topic><topic>MEC protein</topic><topic>Medicine and Health Sciences</topic><topic>Mutation</topic><topic>Neutrophils</topic><topic>Nosocomial infection</topic><topic>Pathogens</topic><topic>Pharmaceutical sciences</topic><topic>Phenols</topic><topic>Phenotype</topic><topic>Plasmids</topic><topic>Proteins</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Bacterial - genetics</topic><topic>Species</topic><topic>Standard deviation</topic><topic>Staphylococcus</topic><topic>Staphylococcus - 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We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. Here, we examined whether the regulatory role of psm-mec on host bacterial virulence properties is conserved among other staphylococcal species, S. epidermidis and S. haemolyticus, both of which are important causes of nosocomial infections. In S. epidermidis, introduction of psm-mec decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation. Introduction of psm-mec with a stop-codon mutation that did not express PSM-mec protein but did express psm-mec RNA also decreased PSM production, but did not increase biofilm formation. Thus, the psm-mec RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in S. epidermidis. In S. haemolyticus, introduction of psm-mec decreased PSM production, but did not affect biofilm formation. The mutated psm-mec with a stop-codon also caused the same effect. Thus, the psm-mec RNA also inhibits PSM production in S. haemolyticus. These findings suggest that the inhibitory role of psm-mec RNA on exotoxin production is conserved among staphylococcal species, although the stimulating effect of the psm-mec gene on biofilm formation is not conserved.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24926994</pmid><doi>10.1371/journal.pone.0100260</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2014-06, Vol.9 (6), p.e100260-e100260 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1978567260 |
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| subjects | Antibiotic resistance Antibiotics Bacteria Biofilms Biofilms - growth & development Biology and Life Sciences Conserved Sequence Drug resistance Exotoxins Exotoxins - genetics Gene Expression Regulation, Bacterial Gene Silencing - physiology Genes Genomes Gram-positive bacteria Health aspects Hospitals Interspersed Repetitive Sequences - physiology Laboratories Mec gene MEC protein Medicine and Health Sciences Mutation Neutrophils Nosocomial infection Pathogens Pharmaceutical sciences Phenols Phenotype Plasmids Proteins Ribonucleic acid RNA RNA, Bacterial - genetics Species Standard deviation Staphylococcus Staphylococcus - genetics Staphylococcus - growth & development Staphylococcus - pathogenicity Staphylococcus aureus Staphylococcus aureus - genetics Staphylococcus aureus - growth & development Staphylococcus epidermidis Staphylococcus epidermidis - genetics Staphylococcus epidermidis - growth & development Staphylococcus epidermidis - pathogenicity Staphylococcus haemolyticus - genetics Staphylococcus haemolyticus - growth & development Staphylococcus haemolyticus - pathogenicity Staphylococcus infections Toxins Transposons Virulence Virulence (Microbiology) Virulence - genetics Wildlife conservation |
| title | Inhibition of exotoxin production by mobile genetic element SCCmec-encoded psm-mec RNA is conserved in staphylococcal species |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-29T00%3A40%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20exotoxin%20production%20by%20mobile%20genetic%20element%20SCCmec-encoded%20psm-mec%20RNA%20is%20conserved%20in%20staphylococcal%20species&rft.jtitle=PloS%20one&rft.au=Ikuo,%20Mariko&rft.date=2014-06-13&rft.volume=9&rft.issue=6&rft.spage=e100260&rft.epage=e100260&rft.pages=e100260-e100260&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0100260&rft_dat=%3Cgale_plos_%3EA418552410%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c688t-e8fb43770f458c6572326ebc3435312b2196a694b9f65cf6d564ed1a1f323fa43%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1978567260&rft_id=info:pmid/24926994&rft_galeid=A418552410&rfr_iscdi=true |