ArticleJournal of bacteriology2005
Simultaneous deficiency of both MurA and p60 proteins generates a rough phenotype in Listeria monocytogenes.
Article in Journal of bacteriology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 69 citations in OpenAlex.
- On the role of cell chaining in the attenuation of aVirulence · 2026Article
- Heparin-binding enhances extracellular listeriolysin O activity, overcoming cholesterol inhibition and pH dependence.Journal of bacteriology · 2026Article
- Identification of a fungal antibacterial endopeptidase that cleaves peptidoglycan.EMBO reports · 2025Article
- Aquatic environment drives the emergence of cell wall-deficient dormant forms in Listeria.Nature communications · 2024Article
- LygA retention on the surface of Listeria monocytogenes via its interaction with wall teichoic acid modulates bacterial homeostasis and virulence.PLoS pathogens · 2023Article
- SecA2 Associates with Translating Ribosomes and Contributes to the Secretion of Potent IFN-β Inducing RNAs.International journal of molecular sciences · 2022Article
- Discovery of MurA Inhibitors as Novel Antimicrobials through an Integrated Computational and Experimental Approach.Antibiotics (Basel, Switzerland) · 2022Article
- A Novel Phage Indirectly Regulates Diatom Growth by Infecting a Diatom-Associated Biofilm-Forming Bacterium.Applied and environmental microbiology · 2022Article
- Biofilm Formation byApplied and environmental microbiology · 2021Article
- Artificial Selection for Pathogenicity Mutations inInfection and immunity · 2019Article
- Cell Wall Hydrolases in Bacteria: Insight on the Diversity of Cell Wall Amidases, Glycosidases and Peptidases Toward Peptidoglycan.Frontiers in microbiology · 2019Review
- Is the LysM domain of L. monocytogenes p60 protein suitable for engineering a protein with high peptidoglycan binding affinity?Bioengineered · 2016Article
- A prl mutation in SecY suppresses secretion and virulence defects of Listeria monocytogenes secA2 mutants.Journal of bacteriology · 2015Article
- The p60 and NamA autolysins from Listeria monocytogenes contribute to host colonization and induction of protective memory.Cellular microbiology · 2015Article
- Intra- and inter-species interactions within biofilms of important foodborne bacterial pathogens.Frontiers in microbiology · 2015Review
- Discrete and overlapping functions of peptidoglycan synthases in growth, cell division and virulence of Listeria monocytogenes.Molecular microbiology · 2015Article
- A systematic proteomic analysis of Listeria monocytogenes house-keeping protein secretion systems.Molecular & cellular proteomics : MCP · 2014Article
- Membrane chaperone SecDF plays a role in the secretion of Listeria monocytogenes major virulence factors.Journal of bacteriology · 2013Article
- Article
- A combined use of autolysin p60 and listeriolysin O antigens induces high protective immune responses against Listeria monocytogenes infection.Current microbiology · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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