Bioenergetic Mechanism for Nisin Resistance, Induced by the Acid Tolerance Response of
            <i>Listeria monocytogenes</i>

Bonnet, Marcelo; Rafi, Mohamed; Chikindas, Michael L.; Montville, Thomas J.

doi:10.1128/aem.72.4.2556-2563.2006

Cited by 35 publications

(23 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In aerobic organisms, such as E. coli and Bacillus subtilis, the F 0 F 1 ATPase mainly functions in ATP synthesis (33). Interestingly, in L. monocytogenes the F 0 F 1 ATPase is down-regulated during an ATR to save ATP, since these bacteria lack a functional respiratory chain (2). In C. glutamicum, the ATPase might be down-regulated to restrict proton influx under acidic conditions.…”

Section: Resultsmentioning

confidence: 99%

Gene Expression Analysis of Corynebacterium glutamicum Subjected to Long-Term Lactic Acid Adaptation

et al. 2007

View full text Add to dashboard Cite

Corynebacteria form an important part of the red smear cheese microbial surface consortium. To gain a better understanding of molecular adaptation due to low pH induced by lactose fermentation, the global gene expression profile of Corynebacterium glutamicum adapted to pH 5.7 with lactic acid under continuous growth in a chemostat was characterized by DNA microarray analysis. Expression of a total of 116 genes was increased and that of 90 genes was decreased compared to pH 7.5 without lactic acid, representing 7% of the genes in the genome. The up-regulated genes encode mainly transcriptional regulators, proteins responsible for export, import, and metabolism, and several proteins of unknown function. As much as 45% of the up-regulated open reading frames code for hypothetical proteins. These results were validated using real-time reverse transcription-PCR. To characterize the functions of 38 up-regulated genes, 36 single-crossover disruption mutants were generated and analyzed for their lactic acid sensitivities. However, only a sigB knockout mutant showed a highly significant negative effect on growth at low pH, suggesting a function in organic-acid adaptation. A sigE mutant already displayed growth retardation at neutral pH but grew better at acidic pH than the sigB mutant. The lack of acid-sensitive phenotypes in 34 out of 36 disrupted genes suggests either a considerable redundancy in acid adaptation response or coincidental effects. Other up-regulated genes included genes for ion transporters and metabolic pathways, including carbohydrate and respiratory metabolism. The enhanced expression of the nrd (ribonucleotide reductase) operon and a DNA ATPase repair protein implies a cellular response to combat acid-induced DNA damage. Surprisingly, multiple iron uptake systems (totaling 15% of the genes induced >2-fold) were induced at low pH. This induction was shown to be coincidental and could be attributed to iron-sequestering effects in complex media at low pH.

show abstract

Section: Resultsmentioning

confidence: 99%

Gene Expression Analysis of Corynebacterium glutamicum Subjected to Long-Term Lactic Acid Adaptation

et al. 2007

View full text Add to dashboard Cite

show abstract

“…As a model, we first tested the CAMP nisin, a commercially available CAMP produced by Lactococcus lactis that is routinely used to study the effects of CAMPs on bacteria (5,7,10,31). The MIC of nisin for strain JIR8094 was approximately 90 g/ml (Table 3).…”

Section: Adaptation Of C Difficile To Nisinmentioning

confidence: 99%

Identification of a Genetic Locus Responsible for Antimicrobial Peptide Resistance in Clostridium difficile

2011

View full text Add to dashboard Cite

Clostridium difficile causes chronic intestinal disease, yet little is understood about how the bacterium interacts with and survives in the host. To colonize the intestine and cause persistent disease, the bacterium must circumvent killing by host innate immune factors, such as cationic antimicrobial peptides (CAMPs). In this study, we investigated the effect of model CAMPs on growth and found that C. difficile is not only sensitive to these compounds but also responds to low levels of CAMPs by expressing genes that lead to CAMP resistance. By plating the bacterium on medium containing the CAMP nisin, we isolated a mutant capable of growing in three times the inhibitory concentration of CAMPs. This mutant also showed increased resistance to the CAMPs gallidermin and polymyxin B, demonstrating tolerance to different types of antimicrobial peptides. We identified the mutated gene responsible for the resistance phenotype as CD1352. This gene encodes a putative orphan histidine kinase that lies adjacent to a predicted ABC transporter operon (CD1349 to CD1351). Transcriptional analysis of the ABC transporter genes revealed that this operon was upregulated in the presence of nisin in wild-type cells and was more highly expressed in the CD1352 mutant. The insertional disruption of the CD1349 gene resulted in significant decreases in resistance to the CAMPs nisin and gallidermin but not polymyxin B. Because of their role in cationic antimicrobial peptide resistance, we propose the designation cprABC for genes CD1349 to CD1351 and cprK for the CD1352 gene. These results provide the first evidence of a C. difficile gene associated with antimicrobial peptide resistance.

show abstract

“…To date, loci that have been implicated in nisin tolerance include the alternative stress sigma factor SigB, the class three stress gene regulator CtsR, the two-component systems LisRK and HK1027, and a penicillin binding protein, Pbp (2,6,11,15,21). In addition, several studies have uncovered a link between the acid stress response of L. monocytogenes and nisin resistance (3,17,24). Several systems are employed by L. monocytogenes to withstand low pH stress, but the glutamate decarboxylase (GAD) system is probably the most important (an overview of the GAD system is in Fig.…”

mentioning

confidence: 99%

Glutamate Decarboxylase-Mediated Nisin Resistance in Listeria monocytogenes

Begley

Cotter

Hill

et al. 2010

Appl Environ Microbiol

View full text Add to dashboard Cite

Analysis of a complete set of glutamate decarboxylase (gad) mutants of Listeria monocytogenes strain LO28 (⌬gadD1, ⌬gadDT1, ⌬gadD2, ⌬gadT2, and ⌬gadD3 mutants) revealed that the ⌬gadD1 mutant is impaired in its ability to tolerate exposure to both sublethal and lethal levels of the lantibiotic nisin. gadD1 is strain variable and is found only in approximately 50% of L. monocytogenes strains. Growth and survival experiments revealed that possession of gadD1 correlates with a higher degree of tolerance to nisin. Significantly, a similar finding using a gadB mutant of L. lactis IL1403 implies that this may be a general phenomenon in Grampositive bacteria. Our findings thus suggest that the specific inhibition of GAD activity or a reduction in the levels of free glutamate may prevent the growth of otherwise resistant GAD ؉ bacteria in foods where low pH and/or nisin is used as a preservative.

show abstract

Bioenergetic Mechanism for Nisin Resistance, Induced by the Acid Tolerance Response of Listeria monocytogenes

Cited by 35 publications

References 40 publications

Gene Expression Analysis of Corynebacterium glutamicum Subjected to Long-Term Lactic Acid Adaptation

Gene Expression Analysis of Corynebacterium glutamicum Subjected to Long-Term Lactic Acid Adaptation

Identification of a Genetic Locus Responsible for Antimicrobial Peptide Resistance in Clostridium difficile

Glutamate Decarboxylase-Mediated Nisin Resistance in Listeria monocytogenes

Contact Info

Product

Resources

About