Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase
Porphyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) homeostasis and surmount nitric oxide stress from host immune responses or other oral bacteria to survive in the periodontal pocket. To determine the involvement of a putative hydroxylamine reductas...
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Veröffentlicht in: | Journal of Bacteriology 2012-03, Vol.194 (6), p.1582-1592 |
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description | Porphyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) homeostasis and surmount nitric oxide stress from host immune responses or other oral bacteria to survive in the periodontal pocket. To determine the involvement of a putative hydroxylamine reductase (PG0893) and a putative nitrite reductase-related protein (PG2213) in P. gingivalis W83 NO stress resistance, genes encoding those proteins were inactivated by allelic exchange mutagenesis. The isogenic mutants P. gingivalis FLL455 (PG0893::ermF) and FLL456 (PG2213::ermF) were black pigmented and showed growth rates and gingipain and hemolytic activities similar to those of the wild-type strain. P. gingivalis FLL455 was more sensitive to NO than the wild type. Complementation of P. gingivalis FLL455 with the wild-type gene restored the level of NO sensitivity to a level similar to that of the parent strain. P. gingivalis FLL455 and FLL456 showed sensitivity to oxidative stress similar to that of the wild-type strain. DNA microarray analysis showed that PG0893 and PG2213 were upregulated 1.4- and 2-fold, respectively, in cells exposed to NO. In addition, 178 genes were upregulated and 201 genes downregulated more than 2-fold. The majority of these modulated genes were hypothetical or of unknown function. PG1181, predicted to encode a transcriptional regulator, was upregulated 76-fold. Transcriptome in silico analysis of the microarray data showed major metabolomic variations in key pathways. Collectively, these findings indicate that PG0893 and several other genes may play an important role in P. gingivalis NO stress resistance. |
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To determine the involvement of a putative hydroxylamine reductase (PG0893) and a putative nitrite reductase-related protein (PG2213) in P. gingivalis W83 NO stress resistance, genes encoding those proteins were inactivated by allelic exchange mutagenesis. The isogenic mutants P. gingivalis FLL455 (PG0893::ermF) and FLL456 (PG2213::ermF) were black pigmented and showed growth rates and gingipain and hemolytic activities similar to those of the wild-type strain. P. gingivalis FLL455 was more sensitive to NO than the wild type. Complementation of P. gingivalis FLL455 with the wild-type gene restored the level of NO sensitivity to a level similar to that of the parent strain. P. gingivalis FLL455 and FLL456 showed sensitivity to oxidative stress similar to that of the wild-type strain. DNA microarray analysis showed that PG0893 and PG2213 were upregulated 1.4- and 2-fold, respectively, in cells exposed to NO. In addition, 178 genes were upregulated and 201 genes downregulated more than 2-fold. The majority of these modulated genes were hypothetical or of unknown function. PG1181, predicted to encode a transcriptional regulator, was upregulated 76-fold. Transcriptome in silico analysis of the microarray data showed major metabolomic variations in key pathways. Collectively, these findings indicate that PG0893 and several other genes may play an important role in P. gingivalis NO stress resistance.</description><identifier>ISSN: 0021-9193</identifier><identifier>EISSN: 1098-5530</identifier><identifier>EISSN: 1067-8832</identifier><identifier>DOI: 10.1128/jb.06457-11</identifier><identifier>PMID: 22247513</identifier><identifier>CODEN: JOBAAY</identifier><language>eng</language><publisher>Washington, DC: American Society for Microbiology</publisher><subject>adults ; bacteria ; Bacteriology ; Biological and medical sciences ; DNA microarrays ; Drug Resistance, Bacterial ; Fundamental and applied biological sciences. Psychology ; Gene Deletion ; Gene expression ; Gene Expression Profiling ; gene expression regulation ; Gene Expression Regulation, Bacterial ; genes ; Genetic Complementation Test ; gingipain ; Gram-negative bacteria ; Homeostasis ; immune response ; metabolomics ; Microarray Analysis ; microarray technology ; Microbiology ; Miscellaneous ; mutagenesis ; mutants ; Nitric oxide ; Nitric Oxide - toxicity ; nitrites ; oxidative stress ; Oxidoreductases - genetics ; Oxidoreductases - metabolism ; Porphyromonas gingivalis ; Porphyromonas gingivalis - drug effects ; Porphyromonas gingivalis - enzymology ; Porphyromonas gingivalis - genetics ; Porphyromonas gingivalis - physiology ; Proteins ; stress tolerance ; Stress, Physiological ; transcription factors ; transcriptome</subject><ispartof>Journal of Bacteriology, 2012-03, Vol.194 (6), p.1582-1592</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright American Society for Microbiology Mar 2012</rights><rights>Copyright © 2012, American Society for Microbiology. All Rights Reserved. 2012 American Society for Microbiology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c586t-c343ddb526fb3bab9c75996475d0a07db904e5a7d23fdfab5f6a29a169a6ce423</citedby><cites>FETCH-LOGICAL-c586t-c343ddb526fb3bab9c75996475d0a07db904e5a7d23fdfab5f6a29a169a6ce423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294835/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294835/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25639014$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22247513$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Boutrin, Marie-Claire</creatorcontrib><creatorcontrib>Wang, Charles</creatorcontrib><creatorcontrib>Aruni, Wilson</creatorcontrib><creatorcontrib>Li, Xiaojin</creatorcontrib><creatorcontrib>Fletcher, Hansel M</creatorcontrib><title>Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase</title><title>Journal of Bacteriology</title><addtitle>J Bacteriol</addtitle><description>Porphyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) homeostasis and surmount nitric oxide stress from host immune responses or other oral bacteria to survive in the periodontal pocket. To determine the involvement of a putative hydroxylamine reductase (PG0893) and a putative nitrite reductase-related protein (PG2213) in P. gingivalis W83 NO stress resistance, genes encoding those proteins were inactivated by allelic exchange mutagenesis. The isogenic mutants P. gingivalis FLL455 (PG0893::ermF) and FLL456 (PG2213::ermF) were black pigmented and showed growth rates and gingipain and hemolytic activities similar to those of the wild-type strain. P. gingivalis FLL455 was more sensitive to NO than the wild type. Complementation of P. gingivalis FLL455 with the wild-type gene restored the level of NO sensitivity to a level similar to that of the parent strain. P. gingivalis FLL455 and FLL456 showed sensitivity to oxidative stress similar to that of the wild-type strain. DNA microarray analysis showed that PG0893 and PG2213 were upregulated 1.4- and 2-fold, respectively, in cells exposed to NO. In addition, 178 genes were upregulated and 201 genes downregulated more than 2-fold. The majority of these modulated genes were hypothetical or of unknown function. PG1181, predicted to encode a transcriptional regulator, was upregulated 76-fold. Transcriptome in silico analysis of the microarray data showed major metabolomic variations in key pathways. Collectively, these findings indicate that PG0893 and several other genes may play an important role in P. gingivalis NO stress resistance.</description><subject>adults</subject><subject>bacteria</subject><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>DNA microarrays</subject><subject>Drug Resistance, Bacterial</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Deletion</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>gene expression regulation</subject><subject>Gene Expression Regulation, Bacterial</subject><subject>genes</subject><subject>Genetic Complementation Test</subject><subject>gingipain</subject><subject>Gram-negative bacteria</subject><subject>Homeostasis</subject><subject>immune response</subject><subject>metabolomics</subject><subject>Microarray Analysis</subject><subject>microarray technology</subject><subject>Microbiology</subject><subject>Miscellaneous</subject><subject>mutagenesis</subject><subject>mutants</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - toxicity</subject><subject>nitrites</subject><subject>oxidative stress</subject><subject>Oxidoreductases - genetics</subject><subject>Oxidoreductases - metabolism</subject><subject>Porphyromonas gingivalis</subject><subject>Porphyromonas gingivalis - drug effects</subject><subject>Porphyromonas gingivalis - enzymology</subject><subject>Porphyromonas gingivalis - genetics</subject><subject>Porphyromonas gingivalis - physiology</subject><subject>Proteins</subject><subject>stress tolerance</subject><subject>Stress, Physiological</subject><subject>transcription factors</subject><subject>transcriptome</subject><issn>0021-9193</issn><issn>1098-5530</issn><issn>1067-8832</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0s1rFDEYBvBBFLtWT941FQqCTM33TC6CFrWVaou15_BOktnNMjNZk5lt97837a714xRCfjy8yZOieE7wESG0frtsjrDkoioJeVDMCFZ1KQTDD4sZxpSUiii2VzxJaYkx4VzQx8UepZRXgrBZ0X3zY_QGnd9469DlGF1K6LtLPo0wGIf8gC5CXC02MfRhgITmfpj7NXQ-odOEvjrrYXQWNRsE6GIaYfRrh042NoabTQe9H1yOs5MZIbmnxaMWuuSe7db94urTxx_HJ-XZ-efT4_dnpRG1HEvDOLO2EVS2DWugUaYSSsk8scWAK9sozJ2AylLW2hYa0UqgCohUII3jlO0X77a5q6npnTVuGCN0ehV9D3GjA3j978ngF3oe1ppRxWsmcsDrXUAMPyeXRt37ZFzXweDClDSRVS04x5Rl-uo_ugxTHPL1tKKyUqqmOKM3W2RiSCm69n4WgvVtifrLB31XYt5l_eLv8e_t79YyONwBSAa6NuaqfPrjhGQqd53dwdYt_Hxx7aPTkHq9bDRRXEtNRH37Vi-3poWgYR5zztUlxUTc_ZaaYPYLI766cw</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Boutrin, Marie-Claire</creator><creator>Wang, Charles</creator><creator>Aruni, Wilson</creator><creator>Li, Xiaojin</creator><creator>Fletcher, Hansel M</creator><general>American Society for Microbiology</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20120301</creationdate><title>Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase</title><author>Boutrin, Marie-Claire ; Wang, Charles ; Aruni, Wilson ; Li, Xiaojin ; Fletcher, Hansel M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c586t-c343ddb526fb3bab9c75996475d0a07db904e5a7d23fdfab5f6a29a169a6ce423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>adults</topic><topic>bacteria</topic><topic>Bacteriology</topic><topic>Biological and medical sciences</topic><topic>DNA microarrays</topic><topic>Drug Resistance, Bacterial</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Deletion</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>gene expression regulation</topic><topic>Gene Expression Regulation, Bacterial</topic><topic>genes</topic><topic>Genetic Complementation Test</topic><topic>gingipain</topic><topic>Gram-negative bacteria</topic><topic>Homeostasis</topic><topic>immune response</topic><topic>metabolomics</topic><topic>Microarray Analysis</topic><topic>microarray technology</topic><topic>Microbiology</topic><topic>Miscellaneous</topic><topic>mutagenesis</topic><topic>mutants</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - toxicity</topic><topic>nitrites</topic><topic>oxidative stress</topic><topic>Oxidoreductases - genetics</topic><topic>Oxidoreductases - metabolism</topic><topic>Porphyromonas gingivalis</topic><topic>Porphyromonas gingivalis - drug effects</topic><topic>Porphyromonas gingivalis - enzymology</topic><topic>Porphyromonas gingivalis - genetics</topic><topic>Porphyromonas gingivalis - physiology</topic><topic>Proteins</topic><topic>stress tolerance</topic><topic>Stress, Physiological</topic><topic>transcription factors</topic><topic>transcriptome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Boutrin, Marie-Claire</creatorcontrib><creatorcontrib>Wang, Charles</creatorcontrib><creatorcontrib>Aruni, Wilson</creatorcontrib><creatorcontrib>Li, Xiaojin</creatorcontrib><creatorcontrib>Fletcher, Hansel M</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of Bacteriology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Boutrin, Marie-Claire</au><au>Wang, Charles</au><au>Aruni, Wilson</au><au>Li, Xiaojin</au><au>Fletcher, Hansel M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase</atitle><jtitle>Journal of Bacteriology</jtitle><addtitle>J Bacteriol</addtitle><date>2012-03-01</date><risdate>2012</risdate><volume>194</volume><issue>6</issue><spage>1582</spage><epage>1592</epage><pages>1582-1592</pages><issn>0021-9193</issn><eissn>1098-5530</eissn><eissn>1067-8832</eissn><coden>JOBAAY</coden><abstract>Porphyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) homeostasis and surmount nitric oxide stress from host immune responses or other oral bacteria to survive in the periodontal pocket. To determine the involvement of a putative hydroxylamine reductase (PG0893) and a putative nitrite reductase-related protein (PG2213) in P. gingivalis W83 NO stress resistance, genes encoding those proteins were inactivated by allelic exchange mutagenesis. The isogenic mutants P. gingivalis FLL455 (PG0893::ermF) and FLL456 (PG2213::ermF) were black pigmented and showed growth rates and gingipain and hemolytic activities similar to those of the wild-type strain. P. gingivalis FLL455 was more sensitive to NO than the wild type. Complementation of P. gingivalis FLL455 with the wild-type gene restored the level of NO sensitivity to a level similar to that of the parent strain. P. gingivalis FLL455 and FLL456 showed sensitivity to oxidative stress similar to that of the wild-type strain. DNA microarray analysis showed that PG0893 and PG2213 were upregulated 1.4- and 2-fold, respectively, in cells exposed to NO. In addition, 178 genes were upregulated and 201 genes downregulated more than 2-fold. The majority of these modulated genes were hypothetical or of unknown function. PG1181, predicted to encode a transcriptional regulator, was upregulated 76-fold. Transcriptome in silico analysis of the microarray data showed major metabolomic variations in key pathways. Collectively, these findings indicate that PG0893 and several other genes may play an important role in P. gingivalis NO stress resistance.</abstract><cop>Washington, DC</cop><pub>American Society for Microbiology</pub><pmid>22247513</pmid><doi>10.1128/jb.06457-11</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | adults bacteria Bacteriology Biological and medical sciences DNA microarrays Drug Resistance, Bacterial Fundamental and applied biological sciences. Psychology Gene Deletion Gene expression Gene Expression Profiling gene expression regulation Gene Expression Regulation, Bacterial genes Genetic Complementation Test gingipain Gram-negative bacteria Homeostasis immune response metabolomics Microarray Analysis microarray technology Microbiology Miscellaneous mutagenesis mutants Nitric oxide Nitric Oxide - toxicity nitrites oxidative stress Oxidoreductases - genetics Oxidoreductases - metabolism Porphyromonas gingivalis Porphyromonas gingivalis - drug effects Porphyromonas gingivalis - enzymology Porphyromonas gingivalis - genetics Porphyromonas gingivalis - physiology Proteins stress tolerance Stress, Physiological transcription factors transcriptome |
title | Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase |
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