BcrC from Bacillus subtilis Acts as an Undecaprenyl Pyrophosphate Phosphatase in Bacitracin Resistance

Bernard, Rémi; Ghachi, Meriem El; Mengin‐Lecreulx, Dominique; Chippaux, Marc; Denizot, François

doi:10.1074/jbc.m413750200

Cited by 90 publications

(96 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, most genes under X control processes contribute to the biosynthesis or metabolism of the cell envelope, including the dlt operon and pbpX (penicillin-binding protein gene), among many others (210). M was found to contribute to bacitracin resistance via regulation of the bcrC (ywoA) gene, encoding a putative bacitracin transport permease (211,212). With respect to nisin resistance, the major contribution of M is expression of ltaSa, encoding a stress-activated lipoteichoic acid synthase.…”

Section: Sigma Factorsmentioning

confidence: 99%

Lantibiotic Resistance

Draper

Cotter

Hill

et al. 2015

Microbiol Mol Biol Rev

132

129

View full text Add to dashboard Cite

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.

show abstract

Section: Sigma Factorsmentioning

confidence: 99%

Lantibiotic Resistance

Draper

Cotter

Hill

et al. 2015

Microbiol Mol Biol Rev

132

129

View full text Add to dashboard Cite

show abstract

“…Other mechanisms, such as the synthesis of alternative isoprenyl pyrophosphate phosphatases or de novo synthesis of undecaprenyl phosphate, have also been described (375,376).…”

Section: Protecting the Cell Envelopementioning

confidence: 99%

Stress Physiology of Lactic Acid Bacteria

Papadimitriou

Alegría

Bron

et al. 2016

Microbiol Mol Biol Rev

515

404

View full text Add to dashboard Cite

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.

show abstract

“…Extracytoplasmic function (ECF) σ factors often control functions related to the cell surface or transport (reviewed by Helmann, 2002 , encodes an undecaprenyl pyrophosphate phosphatase that participates in bacitracin resistance (Cao and Helmann, 2002;Bernard et al ., 2005). The σ X regulon includes two operons that function to decrease the net negative charge of the cell envelope by increasing the synthesis of phosphatidylethanolamine and the D -alanylation of teichoic acids.…”

Section: Introductionmentioning

confidence: 99%

Identification of Bacillus subtilis σ^W‐dependent genes that provide intrinsic resistance to antimicrobial compounds produced by Bacilli

Butcher

Helmann²

2006

Molecular Microbiology

177

184

View full text Add to dashboard Cite

SummaryBacillus subtilis produces many antibiotics of varying structures and specificity. Here we identify a prominent role for s W , an extracytoplasmic function (ECF) sigma factor, in providing intrinsic resistance to antimicrobial compounds produced by other Bacilli . By using a panel of B. subtilis mutants disrupted for each of the 30 known s W -dependent operons we identified resistance genes for at least three different antimicrobial compounds. The ydbST and fosB genes contribute to resistance to antimicrobial compound(s) produced by B. amyloliquefaciens FZB42, the yqeZyqfAB operon provides resistance to the SP b prophage-encoded bacteriocin sublancin, and the yknWXYZ operon and yfhL provide resistance to the antimicrobial peptide SdpC. YfhL encodes a paralogue of SdpI, a membrane protein that provides immunity to SdpC. In competition experiments, we identify s W as a key factor in allowing B. subtilis to resist antibiotic killing and encroachment by competing strains. Together with the previous observation that s W provides inducible resistance against the Streptomyces antibiotic fosfomycin, these studies support the notion that s W controls an antibiosis regulon important in the microbial ecology of soil bacteria.

show abstract

BcrC from Bacillus subtilis Acts as an Undecaprenyl Pyrophosphate Phosphatase in Bacitracin Resistance

Cited by 90 publications

References 38 publications

Lantibiotic Resistance

Lantibiotic Resistance

Stress Physiology of Lactic Acid Bacteria

Identification of Bacillus subtilis σ^W‐dependent genes that provide intrinsic resistance to antimicrobial compounds produced by Bacilli

Contact Info

Product

Resources

About

BcrC from Bacillus subtilis Acts as an Undecaprenyl Pyrophosphate Phosphatase in Bacitracin Resistance

Cited by 90 publications

References 38 publications

Lantibiotic Resistance

Lantibiotic Resistance

Stress Physiology of Lactic Acid Bacteria

Identification of Bacillus subtilis σW‐dependent genes that provide intrinsic resistance to antimicrobial compounds produced by Bacilli

Contact Info

Product

Resources

About

Identification of Bacillus subtilis σ^W‐dependent genes that provide intrinsic resistance to antimicrobial compounds produced by Bacilli