Sequence analysis of rsk, a portion of the 95-kilobase plasmid of Salmonella typhimurium associated with resistance to the bactericidal activity of serum.
Identifieur interne : 001296 ( Ncbi/Merge ); précédent : 001295; suivant : 001297Sequence analysis of rsk, a portion of the 95-kilobase plasmid of Salmonella typhimurium associated with resistance to the bactericidal activity of serum.
Auteurs : J L Vandenbosch ; D K Rabert ; D R Kurlandsky ; G W JonesSource :
- Infection and immunity [ 0019-9567 ] ; 1989.
Descripteurs français
- KwdFr :
- ADN bactérien (génétique), Activité bactéricide du sang, Clonage moléculaire, Données de séquences moléculaires, Gènes bactériens, Masse moléculaire, Plasmides, Protéines bactériennes (génétique), Salmonella typhimurium (génétique), Salmonella typhimurium (pathogénicité), Séquence nucléotidique, Séquences d'acides nucléiques régulatrices.
- MESH :
- génétique : ADN bactérien, Protéines bactériennes, Salmonella typhimurium.
- pathogénicité : Salmonella typhimurium.
- Activité bactéricide du sang, Clonage moléculaire, Données de séquences moléculaires, Gènes bactériens, Masse moléculaire, Plasmides, Séquence nucléotidique, Séquences d'acides nucléiques régulatrices.
English descriptors
- KwdEn :
- Bacterial Proteins (genetics), Base Sequence, Blood Bactericidal Activity, Cloning, Molecular, DNA, Bacterial (genetics), Genes, Bacterial, Molecular Sequence Data, Molecular Weight, Plasmids, Regulatory Sequences, Nucleic Acid, Salmonella typhimurium (genetics), Salmonella typhimurium (pathogenicity).
- MESH :
- chemical , genetics : Bacterial Proteins, DNA, Bacterial.
- genetics : Salmonella typhimurium.
- pathogenicity : Salmonella typhimurium.
- Base Sequence, Blood Bactericidal Activity, Cloning, Molecular, Genes, Bacterial, Molecular Sequence Data, Molecular Weight, Plasmids, Regulatory Sequences, Nucleic Acid.
Abstract
Increased sensitivity to killing by human serum complement occurs in Salmonella typhimurium strains in which the 95-kilobase virulence plasmid is integrated into the chromosome. This phenotypic change appears to be due to alterations in plasmid gene expression and is reversed by the presence of an autonomous plasmid bearing a cloned region of the virulence plasmid. Accordingly, this region has been termed rsk for reduced serum killing. Sequence analysis of the region reveals that rsk is composed of a series of direct 10-base-pair (bp) repeats with a 21-nucleotide periodicity. Two adjacent repeats are identical, but increasing loss of conservation is apparent with increased distance both 5' and 3' of these highly conserved 10-mers. The smallest isolated sequence which restores the serum-resistant phenotype is only 66 bp long and contains the two identical 10-mers and one degenerate 10-mer (8 of 10 bp conserved) 3' of these. The minimal rsk region of 66 bp does not appear to contain a coding sequence, or a promoter, for a structural gene. It is proposed that the minimal rsk is an isolated regulatory site involved in the regulation of the serum resistance of S. typhimurium. Integration of the 95-kilobase plasmid disrupts the normal regulation of virulence plasmid genes, resulting in an increase in the killing of the bacteria by complement activated by the classical pathway. The introduction of the minimal rsk on a multiple-copy plasmid restores resistance to serum killing, possibly through the titration of a trans-acting regulatory factor.
PubMed: 2645213
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pubmed:2645213Le document en format XML
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first="J L" last="Vandenbosch">J L Vandenbosch</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109.</nlm:affiliation><wicri:noCountry code="subField">Ann Arbor 48109</wicri:noCountry></affiliation></author><author><name sortKey="Rabert, D K" sort="Rabert, D K" uniqKey="Rabert D" first="D K" last="Rabert">D K Rabert</name></author><author><name sortKey="Kurlandsky, D R" sort="Kurlandsky, D R" uniqKey="Kurlandsky D" first="D R" last="Kurlandsky">D R Kurlandsky</name></author><author><name sortKey="Jones, G W" sort="Jones, G W" uniqKey="Jones G" first="G W" last="Jones">G W Jones</name></author></analytic><series><title level="j">Infection and immunity</title><idno type="ISSN">0019-9567</idno><imprint><date when="1989" type="published">1989</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bacterial Proteins (genetics)</term><term>Base Sequence</term><term>Blood Bactericidal Activity</term><term>Cloning, Molecular</term><term>DNA, Bacterial (genetics)</term><term>Genes, Bacterial</term><term>Molecular Sequence Data</term><term>Molecular Weight</term><term>Plasmids</term><term>Regulatory Sequences, Nucleic Acid</term><term>Salmonella typhimurium (genetics)</term><term>Salmonella typhimurium (pathogenicity)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ADN bactérien (génétique)</term><term>Activité bactéricide du sang</term><term>Clonage moléculaire</term><term>Données de séquences moléculaires</term><term>Gènes bactériens</term><term>Masse moléculaire</term><term>Plasmides</term><term>Protéines bactériennes (génétique)</term><term>Salmonella typhimurium (génétique)</term><term>Salmonella typhimurium (pathogénicité)</term><term>Séquence nucléotidique</term><term>Séquences d'acides nucléiques régulatrices</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bacterial Proteins</term><term>DNA, Bacterial</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Salmonella typhimurium</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ADN bactérien</term><term>Protéines bactériennes</term><term>Salmonella typhimurium</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Salmonella typhimurium</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Salmonella typhimurium</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Base Sequence</term><term>Blood Bactericidal Activity</term><term>Cloning, Molecular</term><term>Genes, Bacterial</term><term>Molecular Sequence Data</term><term>Molecular Weight</term><term>Plasmids</term><term>Regulatory Sequences, Nucleic Acid</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activité bactéricide du sang</term><term>Clonage moléculaire</term><term>Données de séquences moléculaires</term><term>Gènes bactériens</term><term>Masse moléculaire</term><term>Plasmides</term><term>Séquence nucléotidique</term><term>Séquences d'acides nucléiques régulatrices</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Increased sensitivity to killing by human serum complement occurs in Salmonella typhimurium strains in which the 95-kilobase virulence plasmid is integrated into the chromosome. This phenotypic change appears to be due to alterations in plasmid gene expression and is reversed by the presence of an autonomous plasmid bearing a cloned region of the virulence plasmid. Accordingly, this region has been termed rsk for reduced serum killing. Sequence analysis of the region reveals that rsk is composed of a series of direct 10-base-pair (bp) repeats with a 21-nucleotide periodicity. Two adjacent repeats are identical, but increasing loss of conservation is apparent with increased distance both 5' and 3' of these highly conserved 10-mers. The smallest isolated sequence which restores the serum-resistant phenotype is only 66 bp long and contains the two identical 10-mers and one degenerate 10-mer (8 of 10 bp conserved) 3' of these. The minimal rsk region of 66 bp does not appear to contain a coding sequence, or a promoter, for a structural gene. It is proposed that the minimal rsk is an isolated regulatory site involved in the regulation of the serum resistance of S. typhimurium. Integration of the 95-kilobase plasmid disrupts the normal regulation of virulence plasmid genes, resulting in an increase in the killing of the bacteria by complement activated by the classical pathway. The introduction of the minimal rsk on a multiple-copy plasmid restores resistance to serum killing, possibly through the titration of a trans-acting regulatory factor.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2645213</PMID><DateCompleted><Year>1989</Year><Month>03</Month><Day>29</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0019-9567</ISSN><JournalIssue CitedMedium="Print"><Volume>57</Volume><Issue>3</Issue><PubDate><Year>1989</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Infection and immunity</Title><ISOAbbreviation>Infect. Immun.</ISOAbbreviation></Journal><ArticleTitle>Sequence analysis of rsk, a portion of the 95-kilobase plasmid of Salmonella typhimurium associated with resistance to the bactericidal activity of serum.</ArticleTitle><Pagination><MedlinePgn>850-7</MedlinePgn></Pagination><Abstract><AbstractText>Increased sensitivity to killing by human serum complement occurs in Salmonella typhimurium strains in which the 95-kilobase virulence plasmid is integrated into the chromosome. This phenotypic change appears to be due to alterations in plasmid gene expression and is reversed by the presence of an autonomous plasmid bearing a cloned region of the virulence plasmid. Accordingly, this region has been termed rsk for reduced serum killing. Sequence analysis of the region reveals that rsk is composed of a series of direct 10-base-pair (bp) repeats with a 21-nucleotide periodicity. Two adjacent repeats are identical, but increasing loss of conservation is apparent with increased distance both 5' and 3' of these highly conserved 10-mers. The smallest isolated sequence which restores the serum-resistant phenotype is only 66 bp long and contains the two identical 10-mers and one degenerate 10-mer (8 of 10 bp conserved) 3' of these. The minimal rsk region of 66 bp does not appear to contain a coding sequence, or a promoter, for a structural gene. It is proposed that the minimal rsk is an isolated regulatory site involved in the regulation of the serum resistance of S. typhimurium. Integration of the 95-kilobase plasmid disrupts the normal regulation of virulence plasmid genes, resulting in an increase in the killing of the bacteria by complement activated by the classical pathway. The introduction of the minimal rsk on a multiple-copy plasmid restores resistance to serum killing, possibly through the titration of a trans-acting regulatory factor.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vandenbosch</LastName><ForeName>J L</ForeName><Initials>JL</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rabert</LastName><ForeName>D K</ForeName><Initials>DK</Initials></Author><Author ValidYN="Y"><LastName>Kurlandsky</LastName><ForeName>D R</ForeName><Initials>DR</Initials></Author><Author ValidYN="Y"><LastName>Jones</LastName><ForeName>G W</ForeName><Initials>GW</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI19647</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Infect Immun</MedlineTA><NlmUniqueID>0246127</NlmUniqueID><ISSNLinking>0019-9567</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004269">DNA, Bacterial</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001770" MajorTopicYN="Y">Blood Bactericidal Activity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003001" MajorTopicYN="N">Cloning, Molecular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004269" MajorTopicYN="N">DNA, Bacterial</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005798" MajorTopicYN="Y">Genes, Bacterial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008970" MajorTopicYN="N">Molecular Weight</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010957" MajorTopicYN="Y">Plasmids</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012045" MajorTopicYN="N">Regulatory Sequences, Nucleic Acid</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012486" MajorTopicYN="N">Salmonella typhimurium</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1989</Year><Month>3</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1989</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1989</Year><Month>3</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2645213</ArticleId><ArticleId IdType="pmc">PMC313188</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>EMBO J. 1985 Dec 1;4(12):3333-8</Citation><ArticleIdList><ArticleId 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IdType="pubmed">3517188</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Jones, G W" sort="Jones, G W" uniqKey="Jones G" first="G W" last="Jones">G W Jones</name><name sortKey="Kurlandsky, D R" sort="Kurlandsky, D R" uniqKey="Kurlandsky D" first="D R" last="Kurlandsky">D R Kurlandsky</name><name sortKey="Rabert, D K" sort="Rabert, D K" uniqKey="Rabert D" first="D K" last="Rabert">D K Rabert</name><name sortKey="Vandenbosch, J L" sort="Vandenbosch, J L" uniqKey="Vandenbosch J" first="J L" last="Vandenbosch">J L Vandenbosch</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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