The LisRK signal transduction system determines the sensitivity of Listeria monocytogenes to nisin and cephalosporins

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TY  - JOUR
  - Cotter, PD,Guinane, CM,Hill, C
  - 2002
  - February
  - Antimicrobial Agents and Chemotherapy
  - The LisRK signal transduction system determines the sensitivity of Listeria monocytogenes to nisin and cephalosporins
  - Validated
  - ()
  - PENICILLIN-BINDING PROTEIN GENE-EXPRESSION SYSTEMS GRAM-POSITIVE BACTERIA BETA-LACTAM RESISTANCE PRECURSOR LIPID II STREPTOCOCCUS-PNEUMONIAE LACTOCOCCUS-LACTIS BACILLUS-SUBTILIS TRANSCRIPTIONAL ACTIVATOR LABORATORY MUTANTS
  - 46
  - 2784
  - 2790
  - The Listeria monocytogenes two-component signal transduction system, LisRK, initially identified in strain LO28, plays a significant role in the virulence potential of this important food-borne pathogen. Here, it is shown that, in addition to its major contribution in responding to ethanol, pH, and hydrogen peroxide stresses, LisRK is involved in the ability of the cell to tolerate important antimicrobials used in food and in medicine, e.g., the lantibiotic nisin and the cephalosporin family of antibiotics. A DeltalisK mutant (lacking the LisK histidine kinase sensor component) displays significantly enhanced resistance to the lantibiotic nisin, a greatly enhanced sensitivity to the cephalosporins, and a large reduction in the expression of three genes thought to encode a penicillin-binding protein, another histidine kinase (other than LisK), and a protein of unknown function. Confirmation of the role of LisRK was obtained when the response regulator, LisR, was overexpressed using both constitutive and inducible (nisin-controlled expression) systems. Under these conditions We observed a reversion of the DeltalisK mutant to wild-type growth kinetics in the presence of nisin. It was also found that overexpression of LisR complemented the reduced expression of two of the aforementioned genes. These results demonstrate the important role of LisRK in the response of L. monocytogenes to a number of antimicrobial agents.
  - DOI 10.1128/AAC.46.9.2784-2790.2002
DA  - 2002/02
ER  - 
@article{V160756179,
   = {Cotter,  PD and Guinane,  CM and Hill,  C },
   = {2002},
   = {February},
   = {Antimicrobial Agents and Chemotherapy},
   = {The LisRK signal transduction system determines the sensitivity of Listeria monocytogenes to nisin and cephalosporins},
   = {Validated},
   = {()},
   = {PENICILLIN-BINDING PROTEIN GENE-EXPRESSION SYSTEMS GRAM-POSITIVE BACTERIA BETA-LACTAM RESISTANCE PRECURSOR LIPID II STREPTOCOCCUS-PNEUMONIAE LACTOCOCCUS-LACTIS BACILLUS-SUBTILIS TRANSCRIPTIONAL ACTIVATOR LABORATORY MUTANTS},
   = {46},
  pages = {2784--2790},
   = {{The Listeria monocytogenes two-component signal transduction system, LisRK, initially identified in strain LO28, plays a significant role in the virulence potential of this important food-borne pathogen. Here, it is shown that, in addition to its major contribution in responding to ethanol, pH, and hydrogen peroxide stresses, LisRK is involved in the ability of the cell to tolerate important antimicrobials used in food and in medicine, e.g., the lantibiotic nisin and the cephalosporin family of antibiotics. A DeltalisK mutant (lacking the LisK histidine kinase sensor component) displays significantly enhanced resistance to the lantibiotic nisin, a greatly enhanced sensitivity to the cephalosporins, and a large reduction in the expression of three genes thought to encode a penicillin-binding protein, another histidine kinase (other than LisK), and a protein of unknown function. Confirmation of the role of LisRK was obtained when the response regulator, LisR, was overexpressed using both constitutive and inducible (nisin-controlled expression) systems. Under these conditions We observed a reversion of the DeltalisK mutant to wild-type growth kinetics in the presence of nisin. It was also found that overexpression of LisR complemented the reduced expression of two of the aforementioned genes. These results demonstrate the important role of LisRK in the response of L. monocytogenes to a number of antimicrobial agents.}},
   = {DOI 10.1128/AAC.46.9.2784-2790.2002},
  source = {IRIS}
}
AUTHORSCotter, PD,Guinane, CM,Hill, C
YEAR2002
MONTHFebruary
JOURNAL_CODEAntimicrobial Agents and Chemotherapy
TITLEThe LisRK signal transduction system determines the sensitivity of Listeria monocytogenes to nisin and cephalosporins
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORDPENICILLIN-BINDING PROTEIN GENE-EXPRESSION SYSTEMS GRAM-POSITIVE BACTERIA BETA-LACTAM RESISTANCE PRECURSOR LIPID II STREPTOCOCCUS-PNEUMONIAE LACTOCOCCUS-LACTIS BACILLUS-SUBTILIS TRANSCRIPTIONAL ACTIVATOR LABORATORY MUTANTS
VOLUME46
ISSUE
START_PAGE2784
END_PAGE2790
ABSTRACTThe Listeria monocytogenes two-component signal transduction system, LisRK, initially identified in strain LO28, plays a significant role in the virulence potential of this important food-borne pathogen. Here, it is shown that, in addition to its major contribution in responding to ethanol, pH, and hydrogen peroxide stresses, LisRK is involved in the ability of the cell to tolerate important antimicrobials used in food and in medicine, e.g., the lantibiotic nisin and the cephalosporin family of antibiotics. A DeltalisK mutant (lacking the LisK histidine kinase sensor component) displays significantly enhanced resistance to the lantibiotic nisin, a greatly enhanced sensitivity to the cephalosporins, and a large reduction in the expression of three genes thought to encode a penicillin-binding protein, another histidine kinase (other than LisK), and a protein of unknown function. Confirmation of the role of LisRK was obtained when the response regulator, LisR, was overexpressed using both constitutive and inducible (nisin-controlled expression) systems. Under these conditions We observed a reversion of the DeltalisK mutant to wild-type growth kinetics in the presence of nisin. It was also found that overexpression of LisR complemented the reduced expression of two of the aforementioned genes. These results demonstrate the important role of LisRK in the response of L. monocytogenes to a number of antimicrobial agents.
PUBLISHER_LOCATION
ISBN_ISSN
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DOI_LINKDOI 10.1128/AAC.46.9.2784-2790.2002
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