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J. Bacteriol., Jul 1997, 4123-4128, Vol 179, No. 13
CE Lucas, JT Balthazar, KE Hagman and WM Shafer
Gonococcal resistance to antimicrobial hydrophobic agents (HAs) is due to
energy-dependent removal of HAs from the bacterial cell by the MtrCDE
membrane-associated efflux pump. The mtrR (multiple transferrable
resistance Regulator) gene encodes a putative transcriptional repressor
protein (MtrR) believed to be responsible for regulation of mtrCDE gene
expression. Gel mobility shift and DNase I footprint assays that used a
maltose-binding protein (MBP)-MtrR fusion protein demonstrated that the
MtrR repressor is capable of specifically binding the DNA sequence between
the mtrR and mtrC genes. This binding site was localized to a 26-nucleotide
stretch that includes the promoter utilized for mtrCDE transcription and,
on the complementary strand, a 22-nucleotide stretch that contains the -35
region of the mtrR promoter. A single transition mutation (A-->G) within
the MtrR- binding site decreased the affinity of the target DNA for MtrR
and enhanced gonococcal resistance to HAs when introduced into HA-
susceptible strain FA19 by transformation. Since this mutation enhanced
expression of the mtrCDE gene complex but decreased expression of the mtrR
gene, the data are consistent with the notion that MtrR acts as a
transcriptional repressor of the mtrCDE efflux pump protein genes.
Copyright © 1997, American Society for Microbiology
The MtrR repressor binds the DNA sequence between the mtrR and mtrC genes of Neisseria gonorrhoeae
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
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