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    <!-- http://purl.obolibrary.org/obo/IDO_0100879 -->

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        <rdfs:label xml:lang="en">attenuated disposition</rdfs:label>
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        <rdfs:label xml:lang="en">Brucella pcs mutant</rdfs:label>
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        <rdfs:label>B. suis 1330 pcs mutant</rdfs:label>
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        <ns3:IAO_0000117>YH</ns3:IAO_0000117>
        <rdfs:seeAlso>UniProtKB accession: Q8FW88</rdfs:seeAlso>
        <ns3:IAO_0000119>PMID: 16882035</ns3:IAO_0000119>
        <rdfs:seeAlso>NCBIGene: 1165011</rdfs:seeAlso>
        <rdfs:comment>Information about the mutated molecule: MUTATION: The role of Phosphatidylcholine (PC) in Brucella abortus was examined by generating mutants in pcs (BApcs) and pmtA (BApmtA), which encode key enzymes of the two bacterial PC biosynthetic routes, the choline and methyl-transferase pathways. In rich medium, BApcs and the double mutant BApcspmtA but not BApmtA displayed reduced growth, increased phosphatidylethanolamine and no PC, showing that Pcs is essential for PC synthesis under these conditions. In minimal medium, the parental strain, BApcs and BApmtA showed reduced but significant amounts of PC suggesting that PmtA may also be functional Probing with phage Tb, antibiotics, polycations and serum demonstrated that all mutants had altered envelopes. In macrophages, BApcs and BApcspmtA showed reduced ability to evade fusion with lysosomes and establish a replication niche. In mice, BApcs showed attenuation only at early times after infection, BApmtA at later stages and BApcspmtA throughout. The results suggest that Pcs and PmtA have complementary roles in vivo related to nutrient availability and that PC and the membrane properties that depend on this typical eukaryotic phospholipid are essential for Brucella virulence [Ref6478:Conde-Alvarez et al., 2006].</rdfs:comment>
        <rdfs:comment>The gene pcs from the strain Brucella suis 1330 is a virulence gene.</rdfs:comment>
        <ns3:IAO_0000115>A mutant of strain Brucella suis 1330 that lacks an intact gene pcs.</ns3:IAO_0000115>
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