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The periplasmic protein MppA requires an additional mutated locus to repress marA expression in Escherichia coli
Xiaowen Bina1, Vincent Perreten, Stuart B Levy
1Center for Adaptation Genetics and Drug Resistance, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Abstract:
Escherichia coli strain TP985, which has an insertional mutation in the gene for the periplasmic murein tripeptide binding protein MppA, was previously reported to overproduce MarA and exhibit a multiple-antibiotic resistance (Mar) phenotype (H. Li and J. T. Park, J. Bacteriol. 181:4842-4847, 1999). We found that TP985 contained a previously unrecognized marR mutation which was responsible for the Mar phenotype. Transduction of the mppA mutation from TP985 to another wild-type strain did not affect antibiotic susceptibility. Overproduction of MppA repressed marA transcription in TP985 but not in other mppA or marR mutants. Therefore, TP985 contains an additional unknown mutation(s) that facilitates the repression of marA expression by MppA.
Insights
A previously identified Escherichia coli mutation was found to be caused by an unrecognized marR mutation, leading to multiple-antibiotic resistance. Overproduction of MppA repressed marA transcription, but only in strains with additional unknown mutations.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Escherichia coli strain TP985 was previously reported to overproduce MarA and exhibit a multiple-antibiotic resistance (Mar) phenotype due to an insertional mutation in the mppA gene.
- The mppA gene encodes the periplasmic murein tripeptide binding protein.
Purpose of the Study:
- To investigate the genetic basis of the multiple-antibiotic resistance (Mar) phenotype in Escherichia coli strain TP985.
- To determine the role of MppA overproduction in the regulation of marA transcription and antibiotic resistance.
Main Methods:
- Genetic analysis of Escherichia coli strain TP985 to identify mutations.
- Transduction experiments to transfer mutations between strains.
- Analysis of marA gene transcription and its regulation by MppA.
Main Results:
- The multiple-antibiotic resistance (Mar) phenotype in strain TP985 was attributed to a previously unrecognized marR mutation.
- Transduction of the mppA mutation into a wild-type strain did not alter antibiotic susceptibility.
- Overproduction of MppA repressed marA transcription in TP985, but not in other mppA or marR mutants, indicating the presence of additional mutations in TP985.
Conclusions:
- The Mar phenotype in Escherichia coli TP985 is primarily caused by a marR mutation.
- MppA can repress marA transcription, but this regulatory mechanism is dependent on the presence of additional, yet unidentified, mutations in the TP985 strain.