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        <rdfs:label xml:lang="en">bearer of at some time</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/IDO_0100116 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/IDO_0100116">
        <rdfs:label>Brucella virulence factor disposition</rdfs:label>
    </Class>
    


    <!-- http://purl.obolibrary.org/obo/NCBITaxon_224914 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/NCBITaxon_224914">
        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">Brucella melitensis bv. 1 str. 16M</rdfs:label>
    </Class>
    


    <!-- http://purl.obolibrary.org/obo/OGG_3001198200 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/OGG_3001198200">
        <rdfs:label rdf:datatype="http://www.w3.org/2001/XMLSchema#string">BMEII0428</rdfs:label>
    </Class>
    


    <!-- http://purl.obolibrary.org/obo/PR_000000001 -->

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    <!-- http://purl.obolibrary.org/obo/PR_Q8YCV0 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/PR_Q8YCV0">
        <rdfs:label>D-erythrulose 4-phosphate dehydrogenase</rdfs:label>
        <rdfs:subClassOf rdf:resource="http://purl.obolibrary.org/obo/PR_000000001"/>
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        <rdfs:seeAlso>NCBIProteinGI: 17988773</rdfs:seeAlso>
        <rdfs:seeAlso>NCBIGene: 1198200</rdfs:seeAlso>
        <rdfs:seeAlso>NCBIProteinAccess:NP_541406.1</rdfs:seeAlso>
        <ns3:IAO_0000119>PMID: 10708387, 16177356</ns3:IAO_0000119>
        <rdfs:comment>Gene name: eryC</rdfs:comment>
        <rdfs:comment>Molecule Role Annotation: MUTATION: The eryC gene encodes for enzyme Derythrulose-1-phosphate dehydrogenase. The vaccine strain B abortus B19 is the only known B abortus isolate whose growth is inhibited by erythritol. The B abortus B19 strain is an eryCD double mutant. The defect in B19 was complemented in trans by plasmids containing the complete ery region and by plasmids with Tn1725 insertions in  eryA, eryB and eryD. Plasmids with Tn1725 insertions in eryC were the only ones that failed to complement the Ery phenotype of B19 [Ref6483:Sangari et al., 2000].   Allelic exchange mutants in eryC of Brucella suis were erythritol sensitive in vitro with a MIC of 1 to 5 mM of erythritol. Their multiplication in macrophage-like cells was 50 to 90- fold reduced , but complementation of the  mutant restored wild-type levels of intracellular multiplication and the capacity to use erythritol as a sole carbon source. In vivo, the eryC  mutant colonized the spleens of infected BALBc mice to a significantly lower extent than the wild type and the complemented strain. Interestingly, eryC mutants that were in addition spontaneously erythritol tolerant nevertheless exhibited wild-type-like intramacrophagic and intramurine replication. In conclusion, erythritol was not an essential carbon source for the pathogen in the macrophage host cell but that the inactivation of the eryC gene significantly reduced the intramacrophagic and intramurine fitness of B suis [Ref6551:Burkhardt et al., 2005].</rdfs:comment>
        <rdfs:seeAlso>UniProtKB: PR:Q8YCV0</rdfs:seeAlso>
        <rdfs:comment>This protein is a Brucella virulence factor. MUTATION: The eryC gene encodes for enzyme Derythrulose-1-phosphate dehydrogenase. The vaccine strain B abortus B19 is the only known B abortus isolate whose growth is inhibited by erythritol. The B abortus B19 strain is an eryCD double mutant. The defect in B19 was complemented in trans by plasmids containing the complete ery region and by plasmids with Tn1725 insertions in  eryA, eryB and eryD. Plasmids with Tn1725 insertions in eryC were the only ones that failed to complement the Ery phenotype of B19 [Ref6483:Sangari et al., 2000].   Allelic exchange mutants in eryC of Brucella suis were erythritol sensitive in vitro with a MIC of 1 to 5 mM of erythritol. Their multiplication in macrophage-like cells was 50 to 90- fold reduced , but complementation of the  mutant restored wild-type levels of intracellular multiplication and the capacity to use erythritol as a sole carbon source. In vivo, the eryC  mutant colonized the spleens of infected BALBc mice to a significantly lower extent than the wild type and the complemented strain. Interestingly, eryC mutants that were in addition spontaneously erythritol tolerant nevertheless exhibited wild-type-like intramacrophagic and intramurine replication. In conclusion, erythritol was not an essential carbon source for the pathogen in the macrophage host cell but that the inactivation of the eryC gene significantly reduced the intramacrophagic and intramurine fitness of B suis [Ref6551:Burkhardt et al., 2005].</rdfs:comment>
        <rdfs:seeAlso>LocusTag: BMEII0428</rdfs:seeAlso>
    </Class>
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