<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Smith RE</submitter><funding>Medical Research Council</funding><funding>Biotechnology and Biological Sciences Research Council</funding><funding>Engineering and Physical Sciences Research Council</funding><pagination>e1007730</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6497286</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(5)</volume><pubmed_abstract>Enterococcus faecalis is an opportunistic pathogen with an intrinsically high resistance to lysozyme, a key effector of the innate immune system. This high level of resistance requires a complex network of transcriptional regulators and several genes (oatA, pgdA, dltA and sigV) acting synergistically to inhibit both the enzymatic and cationic antimicrobial peptide activities of lysozyme. We sought to identify novel genes modulating E. faecalis resistance to lysozyme. Random transposon mutagenesis carried out in the quadruple oatA/pgdA/dltA/sigV mutant led to the identification of several independent insertions clustered on the chromosome. These mutations were located in a locus referred to as the enterococcal polysaccharide antigen (EPA) variable region located downstream of the highly con</pubmed_abstract><journal>PLoS pathogens</journal><pubmed_title>Decoration of the enterococcal polysaccharide antigen EPA is essential for virulence, cell surface charge and interaction with effectors of the innate immune system.</pubmed_title><pmcid>PMC6497286</pmcid><funding_grant_id>BB/M011151/1 (Project 1802691)</funding_grant_id><funding_grant_id>BB/R000727/1</funding_grant_id><funding_grant_id>1802691</funding_grant_id><funding_grant_id>BB/M011151/1</funding_grant_id><funding_grant_id>MR/N02995X/1</funding_grant_id><funding_grant_id>EP/S01358X/1</funding_grant_id><pubmed_authors>Prajsnar TK</pubmed_authors><pubmed_authors>Williamson MP</pubmed_authors><pubmed_authors>Mesnage S</pubmed_authors><pubmed_authors>Salamaga B</pubmed_authors><pubmed_authors>Hajdamowicz N</pubmed_authors><pubmed_authors>Fontaine T</pubmed_authors><pubmed_authors>Kolodziejczyk J</pubmed_authors><pubmed_authors>Hounslow AM</pubmed_authors><pubmed_authors>Herry JM</pubmed_authors><pubmed_authors>Smith RE</pubmed_authors><pubmed_authors>Szkuta P</pubmed_authors><pubmed_authors>Bulmer GS</pubmed_authors><pubmed_authors>Serror P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Decoration of the enterococcal polysaccharide antigen EPA is essential for virulence, cell surface charge and interaction with effectors of the innate immune system.</name><description>Enterococcus faecalis is an opportunistic pathogen with an intrinsically high resistance to lysozyme, a key effector of the innate immune system. This high level of resistance requires a complex network of transcriptional regulators and several genes (oatA, pgdA, dltA and sigV) acting synergistically to inhibit both the enzymatic and cationic antimicrobial peptide activities of lysozyme. We sought to identify novel genes modulating E. faecalis resistance to lysozyme. Random transposon mutagenesis carried out in the quadruple oatA/pgdA/dltA/sigV mutant led to the identification of several independent insertions clustered on the chromosome. These mutations were located in a locus referred to as the enterococcal polysaccharide antigen (EPA) variable region located downstream of the highly con</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 May</publication><modification>2025-04-19T22:53:50.683Z</modification><creation>2019-06-06T23:26:28Z</creation></dates><accession>S-EPMC6497286</accession><cross_references><pubmed>31048927</pubmed><doi>10.1371/journal.ppat.1007730</doi></cross_references></HashMap>