Role of murE in the Expression of β-Lactam Antibiotic Resistance in Staphylococcus aureus

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Published inJournal of Bacteriology Vol. 186; no. 6; pp. 1705 - 1713
Main Authors GARDETE, S, LUDOVICE, A. M, SOBRAL, R. G, FILIPE, S. R, DE LENCASTRE, H, TOMASZ, A
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.03.2004
Subjects
Antibiotics
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Bacteriology
beta-Lactam Resistance
beta-Lactams - pharmacology
Biological and medical sciences
Cell Wall - chemistry
Culture Media
Drug resistance
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial
Genes
Isopropyl Thiogalactoside - pharmacology
Methicillin Resistance - genetics
Microbial Sensitivity Tests
Microbiology
Miscellaneous
Molecular Biology of Pathogens
murE gene
Mutation
penicillin-binding protein 2
Peptide Synthases - genetics
Peptide Synthases - metabolism
Peptidoglycan - analysis
Physical growth
Staphylococcus aureus
Staphylococcus aureus - drug effects
Staphylococcus aureus - genetics
Staphylococcus aureus - growth & development
Staphylococcus aureus - metabolism
Transcription, Genetic
Infection
Resistance
Antibiotic
Microbiology
β-Lactams
Bacteriosis
Bacteria
Micrococcales
Micrococcaceae
Staphylococcal infection
Bacteriology
Staphylococcus aureus
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Abstract Article Usage Stats Services JB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue JB About JB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0021-9193 Online ISSN: 1098-5530 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to JB .asm.org, visit: JB       
AbstractList It was shown earlier that Tn551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic reduction in methicillin resistance, accompanied by accumulation of UDP-MurNAc dipeptide in the cell wall precursor pool and incorporation of these abnormal muropeptides into the peptidoglycan of the mutant. Methicillin resistance was recovered in a suppressor mutant. The murE gene of the same strain was then put under the control of the isopropyl-beta-D-thiogalactopyranoside (IPTG)-inducible promoter Pspac. Bacteria grown in the presence of suboptimal concentrations of IPTG accumulated UDP-MurNAc dipeptide in the cell wall precursor pool. Both growth rates and methicillin resistance levels (but not resistance to other antibiotics) were a function of the IPTG concentration. Northern analysis showed a gradual increase in the transcription of murE and also in the transcription of pbpB and mecA, parallel with the increasing concentrations of IPTG in the medium. A similar increase in the transcription of pbpB and mecA, the structural genes of penicillin-binding protein 2 (PBP2) and PBP2A, was also detected in the suppressor mutant. The expression of these two proteins, which are known to play critical roles in the mechanism of staphylococcal methicillin resistance, appears to be--directly or indirectly--under the control of the murE gene. Our data suggest that the drastic reduction of the methicillin MIC seen in the murE mutant may be caused by the insufficient cellular amounts of these two PBPs.[PUBLICATION ABSTRACT]
It was shown earlier that Tn551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic reduction in methicillin resistance, accompanied by accumulation of UDP-MurNAc dipeptide in the cell wall precursor pool and incorporation of these abnormal muropeptides into the peptidoglycan of the mutant. Methicillin resistance was recovered in a suppressor mutant. The murE gene of the same strain was then put under the control of the isopropyl-beta-D-thiogalactopyranoside (IPTG)-inducible promoter P(spac). Bacteria grown in the presence of suboptimal concentrations of IPTG accumulated UDP-MurNAc dipeptide in the cell wall precursor pool. Both growth rates and methicillin resistance levels (but not resistance to other antibiotics) were a function of the IPTG concentration. Northern analysis showed a gradual increase in the transcription of murE and also in the transcription of pbpB and mecA, parallel with the increasing concentrations of IPTG in the medium. A similar increase in the transcription of pbpB and mecA, the structural genes of penicillin-binding protein 2 (PBP2) and PBP2A, was also detected in the suppressor mutant. The expression of these two proteins, which are known to play critical roles in the mechanism of staphylococcal methicillin resistance, appears to be-directly or indirectly-under the control of the murE gene. Our data suggest that the drastic reduction of the methicillin MIC seen in the murE mutant may be caused by the insufficient cellular amounts of these two PBPs.
It was shown earlier that Tn551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic reduction in methicillin resistance, accompanied by accumulation of UDP-MurNAc dipeptide in the cell wall precursor pool and incorporation of these abnormal muropeptides into the peptidoglycan of the mutant. Methicillin resistance was recovered in a suppressor mutant. The murE gene of the same strain was then put under the control of the isopropyl- beta -D-thiogalactopyranoside (IPTG)-inducible promoter P sub(spac). Bacteria grown in the presence of suboptimal concentrations of IPTG accumulated UDP-MurNAc dipeptide in the cell wall precursor pool. Both growth rates and methicillin resistance levels (but not resistance to other antibiotics) were a function of the IPTG concentration. Northern analysis showed a gradual increase in the transcription of murE and also in the transcription of pbpB and mecA, parallel with the increasing concentrations of IPTG in the medium. A similar increase in the transcription of pbpB and mecA, the structural genes of penicillin-binding protein 2 (PBP2) and PBP2A, was also detected in the suppressor mutant. The expression of these two proteins, which are known to play critical roles in the mechanism of staphylococcal methicillin resistance, appears to be: directly or indirectly: under the control of the murE gene. Our data suggest that the drastic reduction of the methicillin MIC seen in the murE mutant may be caused by the insufficient cellular amounts of these two PBPs.
ABSTRACT It was shown earlier that Tn 551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic reduction in methicillin resistance, accompanied by accumulation of UDP-MurNAc dipeptide in the cell wall precursor pool and incorporation of these abnormal muropeptides into the peptidoglycan of the mutant. Methicillin resistance was recovered in a suppressor mutant. The murE gene of the same strain was then put under the control of the isopropyl-β- d -thiogalactopyranoside (IPTG)-inducible promoter P spac . Bacteria grown in the presence of suboptimal concentrations of IPTG accumulated UDP-MurNAc dipeptide in the cell wall precursor pool. Both growth rates and methicillin resistance levels (but not resistance to other antibiotics) were a function of the IPTG concentration. Northern analysis showed a gradual increase in the transcription of murE and also in the transcription of pbpB and mecA , parallel with the increasing concentrations of IPTG in the medium. A similar increase in the transcription of pbpB and mecA , the structural genes of penicillin-binding protein 2 (PBP2) and PBP2A, was also detected in the suppressor mutant. The expression of these two proteins, which are known to play critical roles in the mechanism of staphylococcal methicillin resistance, appears to be—directly or indirectly—under the control of the murE gene. Our data suggest that the drastic reduction of the methicillin MIC seen in the murE mutant may be caused by the insufficient cellular amounts of these two PBPs.
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It was shown earlier that Tn 551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic reduction in methicillin resistance, accompanied by accumulation of UDP-MurNAc dipeptide in the cell wall precursor pool and incorporation of these abnormal muropeptides into the peptidoglycan of the mutant. Methicillin resistance was recovered in a suppressor mutant. The murE gene of the same strain was then put under the control of the isopropyl-β- d -thiogalactopyranoside (IPTG)-inducible promoter P spac . Bacteria grown in the presence of suboptimal concentrations of IPTG accumulated UDP-MurNAc dipeptide in the cell wall precursor pool. Both growth rates and methicillin resistance levels (but not resistance to other antibiotics) were a function of the IPTG concentration. Northern analysis showed a gradual increase in the transcription of murE and also in the transcription of pbpB and mecA , parallel with the increasing concentrations of IPTG in the medium. A similar increase in the transcription of pbpB and mecA , the structural genes of penicillin-binding protein 2 (PBP2) and PBP2A, was also detected in the suppressor mutant. The expression of these two proteins, which are known to play critical roles in the mechanism of staphylococcal methicillin resistance, appears to be—directly or indirectly—under the control of the murE gene. Our data suggest that the drastic reduction of the methicillin MIC seen in the murE mutant may be caused by the insufficient cellular amounts of these two PBPs.
Author A. M. Ludovice
S. R. Filipe
H. de Lencastre
A. Tomasz
S. Gardete
R. G. Sobral
AuthorAffiliation Molecular Genetics Laboratory, Instituto de Tecnologia Química e Biológica da Universidade Nova de Lisboa, 2780 Oeiras, Portugal, 1 Laboratory of Microbiology, The Rockefeller University, New York, New York 10021 2
AuthorAffiliation_xml – name: Molecular Genetics Laboratory, Instituto de Tecnologia Química e Biológica da Universidade Nova de Lisboa, 2780 Oeiras, Portugal, 1 Laboratory of Microbiology, The Rockefeller University, New York, New York 10021 2
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Issue 6
Keywords Infection
Resistance
Antibiotic
Microbiology
β-Lactams
Bacteriosis
Bacteria
Micrococcales
Micrococcaceae
Staphylococcal infection
Bacteriology
Staphylococcus aureus
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Corresponding author. Mailing address: The Rockefeller University, Laboratory of Microbiology, 1230 York Ave., New York, NY 10021. Phone: (212) 327-8278. Fax: (212) 327-8688. E-mail: tomasz@mail.rockefeller.edu.
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SSID ssj0014452
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It was shown earlier that Tn551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a drastic...
ABSTRACT It was shown earlier that Tn 551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes...
It was shown earlier that Tn 551 inserted into the C-terminal region of murE of parental methicillin-resistant Staphylococcus aureus strain COL causes a...
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StartPage 1705
SubjectTerms Antibiotics
Bacterial Proteins - genetics
Bacterial Proteins - metabolism
Bacteriology
beta-Lactam Resistance
beta-Lactams - pharmacology
Biological and medical sciences
Cell Wall - chemistry
Culture Media
Drug resistance
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Bacterial
Genes
Isopropyl Thiogalactoside - pharmacology
Methicillin Resistance - genetics
Microbial Sensitivity Tests
Microbiology
Miscellaneous
Molecular Biology of Pathogens
murE gene
Mutation
penicillin-binding protein 2
Peptide Synthases - genetics
Peptide Synthases - metabolism
Peptidoglycan - analysis
Physical growth
Staphylococcus aureus
Staphylococcus aureus - drug effects
Staphylococcus aureus - genetics
Staphylococcus aureus - growth & development
Staphylococcus aureus - metabolism
Transcription, Genetic
Title Role of murE in the Expression of β-Lactam Antibiotic Resistance in Staphylococcus aureus
URI http://jb.asm.org/content/186/6/1705.abstract
https://www.ncbi.nlm.nih.gov/pubmed/14996801
https://www.proquest.com/docview/227096298
https://search.proquest.com/docview/19258859
https://search.proquest.com/docview/71700866
https://pubmed.ncbi.nlm.nih.gov/PMC355982
Volume 186
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