Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165₁, a P-like fimbriae
Pathogenic Escherichia coli 4787 (O115:KV165) causes septicemia in pigs and expresses the fimbriae F165₁ encoded by the foo operon that belongs to the P fimbrial family. fooI and fooB, encoding specific foo regulators, are divergently transcribed; their intergenic region is responsible for the regul...
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| Veröffentlicht in: | FEMS microbiology letters 2007-12, Vol.277 (1), p.28-36 |
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| creator | Tessier, Marie-Catherine Graveline, Richard Crost, Cécile Desabrais, Julie Annick Martin, Christine Drolet, Marc Harel, Josée |
| description | Pathogenic Escherichia coli 4787 (O115:KV165) causes septicemia in pigs and expresses the fimbriae F165₁ encoded by the foo operon that belongs to the P fimbrial family. fooI and fooB, encoding specific foo regulators, are divergently transcribed; their intergenic region is responsible for the regulation of foo expression. The role of global and local supercoiling (transcription-induced supercoiling within the intergenic region) on the regulation of foo expression was investigated. Expression of fooB was significantly altered when global negative supercoiling was reduced by a mutation that decreases DNA gyrase activity. Deletion of the topA gene, encoding for topoisomerase I that relaxes local negative supercoiling, further reduced fooB expression. This suggests that both global and local supercoiling can significantly affect fooB expression. Moreover, FooI, a positive regulator of fooB expression, has no effect on fooB expression in the topA null mutant. This study showed that divergent transcription from a strong promoter can significantly enhance fooB expression and compensate for the absence of FooI in a wild-type strain. |
| doi_str_mv | 10.1111/j.1574-6968.2007.00919.x |
| format | Article |
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The role of global and local supercoiling (transcription-induced supercoiling within the intergenic region) on the regulation of foo expression was investigated. Expression of fooB was significantly altered when global negative supercoiling was reduced by a mutation that decreases DNA gyrase activity. Deletion of the topA gene, encoding for topoisomerase I that relaxes local negative supercoiling, further reduced fooB expression. This suggests that both global and local supercoiling can significantly affect fooB expression. Moreover, FooI, a positive regulator of fooB expression, has no effect on fooB expression in the topA null mutant. This study showed that divergent transcription from a strong promoter can significantly enhance fooB expression and compensate for the absence of FooI in a wild-type strain.</description><identifier>ISSN: 0378-1097</identifier><identifier>EISSN: 1574-6968</identifier><identifier>DOI: 10.1111/j.1574-6968.2007.00919.x</identifier><identifier>CODEN: FMLED7</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Bacteriology ; Biological and medical sciences ; Deoxyribonucleic acid ; DNA ; DNA topoisomerase ; E coli ; fimbriae ; Fundamental and applied biological sciences. Psychology ; Gene deletion ; Gene expression ; Microbiology ; Molecular and cellular biology ; Molecular genetics ; Mutation ; Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains ; Pathogens ; Pili ; regulation ; Regulators ; Septicemia ; Supercoiling ; TopA gene ; topoisomerase ; Transcription ; Transcription. Transcription factor. Splicing. 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The role of global and local supercoiling (transcription-induced supercoiling within the intergenic region) on the regulation of foo expression was investigated. Expression of fooB was significantly altered when global negative supercoiling was reduced by a mutation that decreases DNA gyrase activity. Deletion of the topA gene, encoding for topoisomerase I that relaxes local negative supercoiling, further reduced fooB expression. This suggests that both global and local supercoiling can significantly affect fooB expression. Moreover, FooI, a positive regulator of fooB expression, has no effect on fooB expression in the topA null mutant. This study showed that divergent transcription from a strong promoter can significantly enhance fooB expression and compensate for the absence of FooI in a wild-type strain.</description><subject>Bacteriology</subject><subject>Biological and medical sciences</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA topoisomerase</subject><subject>E coli</subject><subject>fimbriae</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene deletion</subject><subject>Gene expression</subject><subject>Microbiology</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Mutation</subject><subject>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</subject><subject>Pathogens</subject><subject>Pili</subject><subject>regulation</subject><subject>Regulators</subject><subject>Septicemia</subject><subject>Supercoiling</subject><subject>TopA gene</subject><subject>topoisomerase</subject><subject>Transcription</subject><subject>Transcription. Transcription factor. Splicing. 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Psychology</topic><topic>Gene deletion</topic><topic>Gene expression</topic><topic>Microbiology</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Mutation</topic><topic>Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains</topic><topic>Pathogens</topic><topic>Pili</topic><topic>regulation</topic><topic>Regulators</topic><topic>Septicemia</topic><topic>Supercoiling</topic><topic>TopA gene</topic><topic>topoisomerase</topic><topic>Transcription</topic><topic>Transcription. Transcription factor. Splicing. Rna processing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tessier, Marie-Catherine</creatorcontrib><creatorcontrib>Graveline, Richard</creatorcontrib><creatorcontrib>Crost, Cécile</creatorcontrib><creatorcontrib>Desabrais, Julie Annick</creatorcontrib><creatorcontrib>Martin, Christine</creatorcontrib><creatorcontrib>Drolet, Marc</creatorcontrib><creatorcontrib>Harel, Josée</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><jtitle>FEMS microbiology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tessier, Marie-Catherine</au><au>Graveline, Richard</au><au>Crost, Cécile</au><au>Desabrais, Julie Annick</au><au>Martin, Christine</au><au>Drolet, Marc</au><au>Harel, Josée</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165₁, a P-like fimbriae</atitle><jtitle>FEMS microbiology letters</jtitle><date>2007-12</date><risdate>2007</risdate><volume>277</volume><issue>1</issue><spage>28</spage><epage>36</epage><pages>28-36</pages><issn>0378-1097</issn><eissn>1574-6968</eissn><coden>FMLED7</coden><abstract>Pathogenic Escherichia coli 4787 (O115:KV165) causes septicemia in pigs and expresses the fimbriae F165₁ encoded by the foo operon that belongs to the P fimbrial family. fooI and fooB, encoding specific foo regulators, are divergently transcribed; their intergenic region is responsible for the regulation of foo expression. The role of global and local supercoiling (transcription-induced supercoiling within the intergenic region) on the regulation of foo expression was investigated. Expression of fooB was significantly altered when global negative supercoiling was reduced by a mutation that decreases DNA gyrase activity. Deletion of the topA gene, encoding for topoisomerase I that relaxes local negative supercoiling, further reduced fooB expression. This suggests that both global and local supercoiling can significantly affect fooB expression. Moreover, FooI, a positive regulator of fooB expression, has no effect on fooB expression in the topA null mutant. This study showed that divergent transcription from a strong promoter can significantly enhance fooB expression and compensate for the absence of FooI in a wild-type strain.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><doi>10.1111/j.1574-6968.2007.00919.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | FEMS microbiology letters, 2007-12, Vol.277 (1), p.28-36 |
| issn | 0378-1097 1574-6968 |
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| source | Oxford University Press Journals All Titles (1996-Current); Wiley Online Library Journals Frontfile Complete |
| subjects | Bacteriology Biological and medical sciences Deoxyribonucleic acid DNA DNA topoisomerase E coli fimbriae Fundamental and applied biological sciences. Psychology Gene deletion Gene expression Microbiology Molecular and cellular biology Molecular genetics Mutation Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Pathogens Pili regulation Regulators Septicemia Supercoiling TopA gene topoisomerase Transcription Transcription. Transcription factor. Splicing. Rna processing |
| title | Effects of DNA supercoiling and topoisomerases on the expression of genes coding for F165₁, a P-like fimbriae |
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