Identification and Characterization of a Bacitracin Resistance Network in Enterococcus faecalis

Gebhard, Susanne; Fang, Chong; Shaaly, Aishath; Leslie, David J.; Weimar, Marion R.; Kalamorz, Falk; Carne, Alan; Cook, Gregory M.

doi:10.1128/aac.02111-13

Cited by 53 publications

(98 citation statements)

References 36 publications

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“…Experimental evidence from a number of homologous systems, from B. subtilis, Staphylococcus aureus, Streptococcus mutans, Enterococcus faecalis, and Lactobacillus casei, confirms that this signaling pathway is a general characteristic of the Bce-type modules, and on a number of occasions, this pathway has been associated with lantibiotic resistance (107)(108)(109)(110)(111)(112)(113). For example, in L. lactis, a homologue named LlrG/KinG is found encoded to either side of the gene for a VanZ-like protein.…”

Section: Bcers-like Two-component Systemsmentioning

confidence: 88%

Lantibiotic Resistance

Draper

Cotter

Hill

et al. 2015

Microbiol Mol Biol Rev

135

129

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SUMMARY The dramatic rise in the incidence of antibiotic resistance demands that new therapeutic options will have to be developed. One potentially interesting class of antimicrobials are the modified bacteriocins termed lantibiotics, which are bacterially produced, posttranslationally modified, lanthionine/methyllanthionine-containing peptides. It is interesting that low levels of resistance have been reported for lantibiotics compared with commercial antibiotics. Given that there are very few examples of naturally occurring lantibiotic resistance, attempts have been made to deliberately induce resistance phenotypes in order to investigate this phenomenon. Mechanisms that hinder the action of lantibiotics are often innate systems that react to the presence of any cationic peptides/proteins or ones which result from cell well damage, rather than being lantibiotic specific. Such resistance mechanisms often arise due to altered gene regulation following detection of antimicrobials/cell wall damage by sensory proteins at the membrane. This facilitates alterations to the cell wall or changes in the composition of the membrane. Other general forms of resistance include the formation of spores or biofilms, which are a common mechanistic response to many classes of antimicrobials. In rare cases, bacteria have been shown to possess specific antilantibiotic mechanisms. These are often species specific and include the nisin lytic protein nisinase and the phenomenon of immune mimicry.

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Section: Bcers-like Two-component Systemsmentioning

confidence: 88%

Lantibiotic Resistance

Draper

Cotter

Hill

et al. 2015

Microbiol Mol Biol Rev

135

129

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“…lactis (383), but they have been characterized only for E. faecalis (384), Lb. casei (385), S. mutans (386), and S. thermophilus (387).…”

Section: Protecting the Cell Envelopementioning

confidence: 99%

“…In this organism, TCSs and ABC transporters are not genetically associated. One of the ABC transporters is essential for sensing bacitracin and eliciting a response (384). In response to bacitracin, the BceABRS system of S. mutans (also named MbrABRS) induces its own expression and that of three additional uncharacterized genes (386).…”

Section: Protecting the Cell Envelopementioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

539

404

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SUMMARYLactic acid bacteria (LAB) are important starter, commensal, or pathogenic microorganisms. The stress physiology of LAB has been studied in depth for over 2 decades, fueled mostly by the technological implications of LAB robustness in the food industry. Survival of probiotic LAB in the host and the potential relatedness of LAB virulence to their stress resilience have intensified interest in the field. Thus, a wealth of information concerning stress responses exists today for strains as diverse as starter (e.g.,Lactococcus lactis), probiotic (e.g., severalLactobacillusspp.), and pathogenic (e.g.,EnterococcusandStreptococcusspp.) LAB. Here we present the state of the art for LAB stress behavior. We describe the multitude of stresses that LAB are confronted with, and we present the experimental context used to study the stress responses of LAB, focusing on adaptation, habituation, and cross-protection as well as on self-induced multistress resistance in stationary phase, biofilms, and dormancy. We also consider stress responses at the population and single-cell levels. Subsequently, we concentrate on the stress defense mechanisms that have been reported to date, grouping them according to their direct participation in preserving cell energy, defending macromolecules, and protecting the cell envelope. Stress-induced responses of probiotic LAB and commensal/pathogenic LAB are highlighted separately due to the complexity of the peculiar multistress conditions to which these bacteria are subjected in their hosts. Induction of prophages under environmental stresses is then discussed. Finally, we present systems-based strategies to characterize the “stressome” of LAB and to engineer new food-related and probiotic LAB with improved stress tolerance.

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“…In order to study the contribution of the BceRS system towards resistance against SDP, we first performed growth measurements of WT and a mutant carrying unmarked deletions of all three Bce-like systems (DbceRSAB DpsdRSAB DyxdJKLM-yxeA) of B. subtilis W168 (Gebhard et al, 2014) (TMB1518, referred to as the 'D3|bce' mutant hereafter) shown in Fig. 5(a).…”

Section: Bcers System Does Not Mediate Resistance Against Cannibalismmentioning

confidence: 99%

Cannibalism stress response in Bacillus subtilis

et al. 2016

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When faced with carbon source limitation, the Gram-positive soil organism Bacillus subtilis initiates a survival strategy called sporulation, which leads to the formation of highly resistant endospores that allow B. subtilis to survive even long periods of starvation. In order to avoid commitment to this energy-demanding and irreversible process, B. subtilis employs another strategy called 'cannibalism' to delay sporulation as long as possible. Cannibalism involves the production and secretion of two cannibalism toxins, sporulation delaying protein (SDP) and sporulation killing factor (SKF), which are able to lyse sensitive siblings. The lysed cells are thought to then provide nutrients for the cannibals to slow down or even prevent them from entering sporulation. In this study, we uncovered the role of the cell envelope stress response (CESR), especially the Bce-like antimicrobial peptide detoxification modules, in the cannibalism stress response during the stationary phase. SDP and SKF specifically induce Bce-like systems and some extracytoplasmic function s factors in stationary-phase cultures, but only the latter provide some degree of protection. A full Bce response is only triggered by mature toxins, and not by toxin precursors. Our study provides insights into the close relationship between stationary-phase survival and the CESR of B. subtilis.

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Identification and Characterization of a Bacitracin Resistance Network in Enterococcus faecalis

Cited by 53 publications

References 36 publications

Lantibiotic Resistance

Lantibiotic Resistance

Stress Physiology of Lactic Acid Bacteria

Cannibalism stress response in Bacillus subtilis

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