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Comparative analysis of two-component signal transduction systems of Bacillus cereus, Bacillus thuringiensis and Bacillus anthracis.

Identifieur interne : 000273 ( Main/Exploration ); précédent : 000272; suivant : 000274

Comparative analysis of two-component signal transduction systems of Bacillus cereus, Bacillus thuringiensis and Bacillus anthracis.

Auteurs : Mark De Been [Pays-Bas] ; Christof Francke [Pays-Bas] ; Roy Moezelaar [Pays-Bas] ; Tjakko Abee [Pays-Bas] ; Roland J. Siezen [Pays-Bas]

Source :

RBID : pubmed:17005984

Descripteurs français

English descriptors

Abstract

Members of the Bacillus cereus group are ubiquitously present in the environment and can adapt to a wide range of environmental fluctuations. In bacteria, these adaptive responses are generally mediated by two-component signal transduction systems (TCSs), which consist of a histidine kinase (HK) and its cognate response regulator (RR). With the use of in silico techniques, a complete set of HKs and RRs was recovered from eight completely sequenced B. cereus group genomes. By applying a bidirectional best-hits method combined with gene neighbourhood analysis, a footprint of these proteins was made. Around 40 HK-RR gene pairs were detected in each member of the B. cereus group. In addition, each member contained many HK and RR genes not encoded in pairs ("orphans"). Classification of HKs and RRs based on their enzymic domains together with the analysis of two neighbour-joining trees of these domains revealed putative interaction partners for most of the "orphans". Putative biological functions, including involvement in virulence and host-microbe interactions, were predicted for the B. cereus group HKs and RRs by comparing them with those of B. subtilis and other micro-organisms. Remarkably, B. anthracis appeared to lack specific HKs and RRs and was found to contain many truncated, putatively non-functional, HK and RR genes. It is hypothesized that specialization of B. anthracis as a pathogen could have reduced the range of environmental stimuli to which it is exposed. This may have rendered some of its TCSs obsolete, ultimately resulting in the deletion of some HK and RR genes.

DOI: 10.1099/mic.0.29137-0
PubMed: 17005984


Affiliations:


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Le document en format XML

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<term>Adaptation, Physiological (genetics)</term>
<term>Bacillus anthracis (genetics)</term>
<term>Bacillus anthracis (metabolism)</term>
<term>Bacillus anthracis (pathogenicity)</term>
<term>Bacillus cereus (genetics)</term>
<term>Bacillus cereus (metabolism)</term>
<term>Bacillus cereus (pathogenicity)</term>
<term>Bacillus thuringiensis (genetics)</term>
<term>Bacillus thuringiensis (metabolism)</term>
<term>Bacillus thuringiensis (pathogenicity)</term>
<term>Bacterial Proteins (genetics)</term>
<term>Computational Biology (MeSH)</term>
<term>Genes, Regulator (MeSH)</term>
<term>Genome, Bacterial (MeSH)</term>
<term>Histidine Kinase (MeSH)</term>
<term>Protein Kinases (genetics)</term>
<term>Signal Transduction (genetics)</term>
<term>Virulence (genetics)</term>
</keywords>
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<term>Adaptation physiologique (génétique)</term>
<term>Bacillus anthracis (génétique)</term>
<term>Bacillus anthracis (métabolisme)</term>
<term>Bacillus anthracis (pathogénicité)</term>
<term>Bacillus cereus (génétique)</term>
<term>Bacillus cereus (métabolisme)</term>
<term>Bacillus cereus (pathogénicité)</term>
<term>Bacillus thuringiensis (génétique)</term>
<term>Bacillus thuringiensis (métabolisme)</term>
<term>Bacillus thuringiensis (pathogénicité)</term>
<term>Biologie informatique (MeSH)</term>
<term>Gènes régulateurs (MeSH)</term>
<term>Génome bactérien (MeSH)</term>
<term>Histidine kinase (MeSH)</term>
<term>Protein kinases (génétique)</term>
<term>Protéines bactériennes (génétique)</term>
<term>Transduction du signal (génétique)</term>
<term>Virulence (génétique)</term>
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<term>Bacterial Proteins</term>
<term>Protein Kinases</term>
</keywords>
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<term>Adaptation, Physiological</term>
<term>Bacillus anthracis</term>
<term>Bacillus cereus</term>
<term>Bacillus thuringiensis</term>
<term>Signal Transduction</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Adaptation physiologique</term>
<term>Bacillus anthracis</term>
<term>Bacillus cereus</term>
<term>Bacillus thuringiensis</term>
<term>Protein kinases</term>
<term>Protéines bactériennes</term>
<term>Transduction du signal</term>
<term>Virulence</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Bacillus anthracis</term>
<term>Bacillus cereus</term>
<term>Bacillus thuringiensis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Bacillus anthracis</term>
<term>Bacillus cereus</term>
<term>Bacillus thuringiensis</term>
</keywords>
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<term>Bacillus anthracis</term>
<term>Bacillus cereus</term>
<term>Bacillus thuringiensis</term>
</keywords>
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<term>Bacillus cereus</term>
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<term>Histidine Kinase</term>
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<term>Biologie informatique</term>
<term>Gènes régulateurs</term>
<term>Génome bactérien</term>
<term>Histidine kinase</term>
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<div type="abstract" xml:lang="en">Members of the Bacillus cereus group are ubiquitously present in the environment and can adapt to a wide range of environmental fluctuations. In bacteria, these adaptive responses are generally mediated by two-component signal transduction systems (TCSs), which consist of a histidine kinase (HK) and its cognate response regulator (RR). With the use of in silico techniques, a complete set of HKs and RRs was recovered from eight completely sequenced B. cereus group genomes. By applying a bidirectional best-hits method combined with gene neighbourhood analysis, a footprint of these proteins was made. Around 40 HK-RR gene pairs were detected in each member of the B. cereus group. In addition, each member contained many HK and RR genes not encoded in pairs ("orphans"). Classification of HKs and RRs based on their enzymic domains together with the analysis of two neighbour-joining trees of these domains revealed putative interaction partners for most of the "orphans". Putative biological functions, including involvement in virulence and host-microbe interactions, were predicted for the B. cereus group HKs and RRs by comparing them with those of B. subtilis and other micro-organisms. Remarkably, B. anthracis appeared to lack specific HKs and RRs and was found to contain many truncated, putatively non-functional, HK and RR genes. It is hypothesized that specialization of B. anthracis as a pathogen could have reduced the range of environmental stimuli to which it is exposed. This may have rendered some of its TCSs obsolete, ultimately resulting in the deletion of some HK and RR genes.</div>
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<AbstractText>Members of the Bacillus cereus group are ubiquitously present in the environment and can adapt to a wide range of environmental fluctuations. In bacteria, these adaptive responses are generally mediated by two-component signal transduction systems (TCSs), which consist of a histidine kinase (HK) and its cognate response regulator (RR). With the use of in silico techniques, a complete set of HKs and RRs was recovered from eight completely sequenced B. cereus group genomes. By applying a bidirectional best-hits method combined with gene neighbourhood analysis, a footprint of these proteins was made. Around 40 HK-RR gene pairs were detected in each member of the B. cereus group. In addition, each member contained many HK and RR genes not encoded in pairs ("orphans"). Classification of HKs and RRs based on their enzymic domains together with the analysis of two neighbour-joining trees of these domains revealed putative interaction partners for most of the "orphans". Putative biological functions, including involvement in virulence and host-microbe interactions, were predicted for the B. cereus group HKs and RRs by comparing them with those of B. subtilis and other micro-organisms. Remarkably, B. anthracis appeared to lack specific HKs and RRs and was found to contain many truncated, putatively non-functional, HK and RR genes. It is hypothesized that specialization of B. anthracis as a pathogen could have reduced the range of environmental stimuli to which it is exposed. This may have rendered some of its TCSs obsolete, ultimately resulting in the deletion of some HK and RR genes.</AbstractText>
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<PublicationType UI="D016428">Journal Article</PublicationType>
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<Country>England</Country>
<MedlineTA>Microbiology (Reading)</MedlineTA>
<NlmUniqueID>9430468</NlmUniqueID>
<ISSNLinking>1350-0872</ISSNLinking>
</MedlineJournalInfo>
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<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 2.7.-</RegistryNumber>
<NameOfSubstance UI="D011494">Protein Kinases</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 2.7.13.1</RegistryNumber>
<NameOfSubstance UI="D000071677">Histidine Kinase</NameOfSubstance>
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<DescriptorName UI="D001408" MajorTopicYN="N">Bacillus anthracis</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001409" MajorTopicYN="N">Bacillus cereus</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001413" MajorTopicYN="N">Bacillus thuringiensis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D019295" MajorTopicYN="N">Computational Biology</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005809" MajorTopicYN="N">Genes, Regulator</DescriptorName>
</MeshHeading>
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<DescriptorName UI="D016680" MajorTopicYN="N">Genome, Bacterial</DescriptorName>
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<DescriptorName UI="D000071677" MajorTopicYN="N">Histidine Kinase</DescriptorName>
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<MeshHeading>
<DescriptorName UI="D011494" MajorTopicYN="N">Protein Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
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<Year>2006</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2007</Year>
<Month>1</Month>
<Day>25</Day>
<Hour>9</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2006</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>9</Hour>
<Minute>0</Minute>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">17005984</ArticleId>
<ArticleId IdType="doi">10.1099/mic.0.29137-0</ArticleId>
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</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>Pays-Bas</li>
</country>
</list>
<tree>
<country name="Pays-Bas">
<noRegion>
<name sortKey="De Been, Mark" sort="De Been, Mark" uniqKey="De Been M" first="Mark" last="De Been">Mark De Been</name>
</noRegion>
<name sortKey="Abee, Tjakko" sort="Abee, Tjakko" uniqKey="Abee T" first="Tjakko" last="Abee">Tjakko Abee</name>
<name sortKey="Abee, Tjakko" sort="Abee, Tjakko" uniqKey="Abee T" first="Tjakko" last="Abee">Tjakko Abee</name>
<name sortKey="De Been, Mark" sort="De Been, Mark" uniqKey="De Been M" first="Mark" last="De Been">Mark De Been</name>
<name sortKey="De Been, Mark" sort="De Been, Mark" uniqKey="De Been M" first="Mark" last="De Been">Mark De Been</name>
<name sortKey="Francke, Christof" sort="Francke, Christof" uniqKey="Francke C" first="Christof" last="Francke">Christof Francke</name>
<name sortKey="Francke, Christof" sort="Francke, Christof" uniqKey="Francke C" first="Christof" last="Francke">Christof Francke</name>
<name sortKey="Moezelaar, Roy" sort="Moezelaar, Roy" uniqKey="Moezelaar R" first="Roy" last="Moezelaar">Roy Moezelaar</name>
<name sortKey="Moezelaar, Roy" sort="Moezelaar, Roy" uniqKey="Moezelaar R" first="Roy" last="Moezelaar">Roy Moezelaar</name>
<name sortKey="Siezen, Roland J" sort="Siezen, Roland J" uniqKey="Siezen R" first="Roland J" last="Siezen">Roland J. Siezen</name>
<name sortKey="Siezen, Roland J" sort="Siezen, Roland J" uniqKey="Siezen R" first="Roland J" last="Siezen">Roland J. Siezen</name>
<name sortKey="Siezen, Roland J" sort="Siezen, Roland J" uniqKey="Siezen R" first="Roland J" last="Siezen">Roland J. Siezen</name>
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