Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
24
pubmed:dateCreated
2005-12-2
pubmed:databankReference
pubmed:abstractText
We examined eight spontaneously occurring rough mutants of Listeria monocytogenes for their ability to express two previously reported autolysins, p60 and MurA. All mutants lack MurA expression and show strongly reduced levels of extracellular p60. One rough strain harbors a variant of the p60 protein with a partially truncated catalytic domain. In seven cases there were shifts in the localization of p60 to the membrane fraction. Mutations within the secA2 gene, encoding an auxiliary protein secretion system paralog, were previously shown to be involved in the smooth-rough phenotypic variation seen with Listeria strains. An isogenic DeltasecA2 EGDe deletion strain displays a strong pleiotropic reduction of p60 and MurA, in addition to a large number of secreted and surface proteins. However, we observed no apparent SecA2 dysfunction in several of the investigated strains as determined by direct sequencing of the secA2 gene and complementation of the DeltasecA2 mutant with the respective allele cloned from the rough mutant. To determine the gene products required for the smooth-rough transition, we created mutants lacking the individual iap and murA genes as well as a Deltaiap DeltamurA double mutant. The double mutant displays a rough phenotype and exhibits many of the properties seen with the DeltasecA2 mutant. Our results implicate p60 and MurA as important determinants in controlling the cell shape of L. monocytogenes. We also identified homologous MurA and SecA2 proteins in other Listeria species. The muramidase in two species, L. innocua and L. welshimeri, shows activity similar to that of the MurA protein in L. monocytogenes.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-10206711, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-10322020, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-10594817, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-10648100, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-10878057, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-11068915, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-11251838, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-11679669, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-12107135, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-12180923, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-12399477, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-12620121, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-12761132, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-14527997, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-1459966, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-14617644, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-15009888, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-15115801, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-15306019, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-15528535, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-1674525, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-1729245, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-1846855, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-1906869, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-2491841, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-2780297, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-3029033, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-8099071, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-8588903, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-8975898, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-9457885, http://linkedlifedata.com/resource/pubmed/commentcorrection/16321943-9573210
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9193
pubmed:author
pubmed:issnType
Print
pubmed:volume
187
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
8385-94
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed-meshheading:16321943-Adenosine Triphosphatases, pubmed-meshheading:16321943-Bacterial Proteins, pubmed-meshheading:16321943-Blotting, Western, pubmed-meshheading:16321943-Codon, Nonsense, pubmed-meshheading:16321943-DNA, Bacterial, pubmed-meshheading:16321943-Gene Deletion, pubmed-meshheading:16321943-Genetic Complementation Test, pubmed-meshheading:16321943-Lipoproteins, pubmed-meshheading:16321943-Listeria monocytogenes, pubmed-meshheading:16321943-Membrane Transport Proteins, pubmed-meshheading:16321943-Microscopy, Electron, pubmed-meshheading:16321943-Molecular Sequence Data, pubmed-meshheading:16321943-Morphogenesis, pubmed-meshheading:16321943-Muramidase, pubmed-meshheading:16321943-N-Acetylmuramoyl-L-alanine Amidase, pubmed-meshheading:16321943-Phenotype, pubmed-meshheading:16321943-Sequence Analysis, DNA, pubmed-meshheading:16321943-Sequence Deletion
pubmed:year
2005
pubmed:articleTitle
Simultaneous deficiency of both MurA and p60 proteins generates a rough phenotype in Listeria monocytogenes.
pubmed:affiliation
Institut für Medizinische Mikrobiologie, Justus-Liebig-Universität, Frankfurter Strasse 107, D-35392 Giessen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't