Transcription in vivo within the replication origin of the Escherichia coli chromosome: a mechanism for activating initiation of replication
Identifieur interne : 000128 ( Istex/Corpus ); précédent : 000127; suivant : 000129Transcription in vivo within the replication origin of the Escherichia coli chromosome: a mechanism for activating initiation of replication
Auteurs : Tsuneaki Asai ; Chi-Pien Chen ; Toshio Nagata ; Mitsuru Takanami ; Mutsuo ImaiSource :
- Molecular and General Genetics MGG [ 0026-8925 ] ; 1992-01-01.
English descriptors
- KwdEn :
- Teeft :
- Amber mutation, Asai, Bacterial strains, Bamhi, Biol, Chromosomal, Chromosome, Coli, Coli chromosome, Copy number, Deletion, Dnaa, Dnaa boxes, Dnaa gene, Dnaa protein, Dnaa strain, Duplex, Duplex opening, Escherichia, Escherichia coli, Escherichia coli chromosome, Fragment, Genet, Hindiii, Initiation event, Kornberg, Leftward, Leftward origin transcripts, Leftward transcription, Minimal oric, Mutation, Negative supercoiling, Nozaki, Nucleic acids, Oric, Oric fragment, Oric fragments, Oric plasmid replication, Oric plasmids, Oric region, Oric sequence, Origin activity, Phage, Plasmid, Polymerase, Positive supercoiling, Present work, Proc natl acad, Promoter, Promoter fragment, Replication, Replication origin, Right side, Rightward, Rightward origin transcription, Rightward origin transcripts, Rightward synthesis, Rightward transcription, Rightward transcripts, Rpob mutations, Sali, Schauzu, Sugimoto, Supercoiled, Supercoiling, Takanami, Transcript, Transcription, Transcription proceeds, Transcriptional, Transcriptional activation, Xhoi, Xhoi sites.
Abstract
Summary: Within the replication origin, oriC, of the Escherichia coli chromosome, novel in vivo transcripts were detected which proceeded rightward and whose production was activated by DnaA protein. In contrast, DnaA protein repressed the previously described ori-L leftward transcription. The former should introduce negative supercoiling, and the latter positive supercoiling, into the 13-mers. The effects of transcription on the initiation of replication were also investigated by making constructs with promoters placed near oriC. Transcription was found to enhance the origin activity only when it was oriented in such a way as to introduce negative supercoiling into the 13-mers. From these results, we propose that transcription within oriC regulates replication initiation by altering the topology of the 13-mer region.
Url:
DOI: 10.1007/BF00279788
Links to Exploration step
ISTEX:AD9801C92D12106E6389F753E8FC96278701FCADLe document en format XML
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From these results, we propose that transcription within oriC regulates replication initiation by altering the topology of the 13-mer region.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Key words</head><item><term>oriC</term></item><item><term>Replication initiation</term></item><item><term>Transcription regulation</term></item><item><term>DnaA protein</term></item><item><term>Transcriptional activation</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Life Sciences</head><item><term>Biochemistry, general</term></item><item><term>Cell Biology</term></item><item><term>Microbial Genetics and Genomics</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991-08-15">Created</change><change when="1992-01-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/1BB-1WH74LZ3-R/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus springer-journals not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Berlin/Heidelberg</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>438</JournalID><JournalPrintISSN>0026-8925</JournalPrintISSN><JournalElectronicISSN>1432-1874</JournalElectronicISSN><JournalTitle>Molecular and General Genetics MGG</JournalTitle><JournalAbbreviatedTitle>Molec. Gen. Genet.</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Life Sciences</JournalSubject><JournalSubject Type="Secondary">Biochemistry, general</JournalSubject><JournalSubject Type="Secondary">Cell Biology</JournalSubject><JournalSubject Type="Secondary">Microbial Genetics and Genomics</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>231</VolumeIDStart><VolumeIDEnd>231</VolumeIDEnd><VolumeIssueCount>3</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd><IssueArticleCount>21</IssueArticleCount><IssueHistory><CoverDate><Year>1992</Year><Month>1</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1992</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art1"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF00279788</ArticleID><ArticleDOI>10.1007/BF00279788</ArticleDOI><ArticleSequenceNumber>1</ArticleSequenceNumber><ArticleTitle Language="En">Transcription in vivo within the replication origin of the <Emphasis Type="Italic">Escherichia coli</Emphasis> chromosome: a mechanism for activating initiation of replication</ArticleTitle><ArticleFirstPage>169</ArticleFirstPage><ArticleLastPage>178</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2004</Year><Month>8</Month><Day>13</Day></RegistrationDate><Received><Year>1991</Year><Month>8</Month><Day>15</Day></Received></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1992</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>438</JournalID><VolumeIDStart>231</VolumeIDStart><VolumeIDEnd>231</VolumeIDEnd><IssueIDStart>2</IssueIDStart><IssueIDEnd>2</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff2"><AuthorName DisplayOrder="Western"><GivenName>Tsuneaki</GivenName><FamilyName>Asai</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Chi-Pien</GivenName><FamilyName>Chen</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Toshio</GivenName><FamilyName>Nagata</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>Mitsuru</GivenName><FamilyName>Takanami</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Mutsuo</GivenName><FamilyName>Imai</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Institute for Virus Research</OrgDivision><OrgName>Kyoto University</OrgName><OrgAddress><Postcode>606</Postcode><City>Sakyo-ku, Kyoto</City><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>Kaohsiung Medical College</OrgName><OrgAddress><City>Kaohsiung</City><Country>Taiwan</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Institute for Chemical Research</OrgDivision><OrgName>Kyoto University</OrgName><OrgAddress><Postcode>611</Postcode><City>Uji</City><Country>Japan</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Cell Biology</OrgDivision><OrgName>University of New Mexico</OrgName><OrgAddress><City>Albuquerque</City><State>87131</State><Country>USA</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Within the replication origin, <Emphasis Type="Italic">oriC</Emphasis>, of the <Emphasis Type="Italic">Escherichia coli</Emphasis> chromosome, novel in vivo transcripts were detected which proceeded rightward and whose production was activated by DnaA protein. In contrast, DnaA protein repressed the previously described <Emphasis Type="Italic">ori</Emphasis>-L leftward transcription. The former should introduce negative supercoiling, and the latter positive supercoiling, into the 13-mers. The effects of transcription on the initiation of replication were also investigated by making constructs with promoters placed near <Emphasis Type="Italic">oriC</Emphasis>. Transcription was found to enhance the origin activity only when it was oriented in such a way as to introduce negative supercoiling into the 13-mers. From these results, we propose that transcription within <Emphasis Type="Italic">oriC</Emphasis> regulates replication initiation by altering the topology of the 13-mer region.</Para></Abstract><KeywordGroup Language="En"><Heading>Key words</Heading><Keyword><Emphasis Type="Italic">oriC</Emphasis></Keyword><Keyword>Replication initiation</Keyword><Keyword>Transcription regulation</Keyword><Keyword>DnaA protein</Keyword><Keyword>Transcriptional activation</Keyword></KeywordGroup><ArticleNote Type="CommunicatedBy"><SimplePara>Communicated by M. Sekiguchi</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Transcription in vivo within the replication origin of the Escherichia coli chromosome: a mechanism for activating initiation of replication</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Transcription in vivo within the replication origin of the Escherichia coli chromosome: a mechanism for activating initiation of replication</title></titleInfo><name type="personal"><namePart type="given">Tsuneaki</namePart><namePart type="family">Asai</namePart><affiliation>Institute for Virus Research, Kyoto University, 606, Sakyo-ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chi-Pien</namePart><namePart type="family">Chen</namePart><affiliation>Department of Microbiology, Kaohsiung Medical College, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Toshio</namePart><namePart type="family">Nagata</namePart><affiliation>Institute for Virus Research, Kyoto University, 606, Sakyo-ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mitsuru</namePart><namePart type="family">Takanami</namePart><affiliation>Institute for Chemical Research, Kyoto University, 611, Uji, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Mutsuo</namePart><namePart type="family">Imai</namePart><affiliation>Institute for Virus Research, Kyoto University, 606, Sakyo-ku, Kyoto, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Berlin/Heidelberg</placeTerm></place><dateCreated encoding="w3cdtf">1991-08-15</dateCreated><dateIssued encoding="w3cdtf">1992-01-01</dateIssued><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Summary: Within the replication origin, oriC, of the Escherichia coli chromosome, novel in vivo transcripts were detected which proceeded rightward and whose production was activated by DnaA protein. In contrast, DnaA protein repressed the previously described ori-L leftward transcription. The former should introduce negative supercoiling, and the latter positive supercoiling, into the 13-mers. The effects of transcription on the initiation of replication were also investigated by making constructs with promoters placed near oriC. Transcription was found to enhance the origin activity only when it was oriented in such a way as to introduce negative supercoiling into the 13-mers. From these results, we propose that transcription within oriC regulates replication initiation by altering the topology of the 13-mer region.</abstract><subject lang="en"><genre>Key words</genre><topic>oriC</topic><topic>Replication initiation</topic><topic>Transcription regulation</topic><topic>DnaA protein</topic><topic>Transcriptional activation</topic></subject><relatedItem type="host"><titleInfo><title>Molecular and General Genetics MGG</title></titleInfo><titleInfo type="abbreviated"><title>Molec. 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