scholarly journals Gene Cloning and Characterization of VcrM, a Na+-Coupled Multidrug Efflux Pump, fromVibrio choleraeNon-O1

2003 ◽  
Vol 47 (6) ◽  
pp. 419-427 ◽  
Author(s):  
Md. Nazmul Huda ◽  
Jing Chen ◽  
Yuji Morita ◽  
Teruo Kuroda ◽  
Tohru Mizushima ◽  
...  

2006 ◽  
Vol 29 (4) ◽  
pp. 801-804 ◽  
Author(s):  
Youichi Yamada ◽  
Sumiko Shiota ◽  
Tohru Mizushima ◽  
Teruo Kuroda ◽  
Tomofusa Tsuchiya


2006 ◽  
Vol 29 (3) ◽  
pp. 554-556 ◽  
Author(s):  
Youichi Yamada ◽  
Koh-ichiro Hideka ◽  
Sumiko Shiota ◽  
Teruo Kuroda ◽  
Tomofusa Tsuchiya


2008 ◽  
Vol 31 (3) ◽  
pp. 516-519 ◽  
Author(s):  
Yusuke Minato ◽  
Fereshteh Shahcheraghi ◽  
Wakano Ogawa ◽  
Teruo Kuroda ◽  
Tomofusa Tsuchiya


2007 ◽  
Vol 30 (10) ◽  
pp. 1962-1964 ◽  
Author(s):  
Yu Ping ◽  
Wakano Ogawa ◽  
Teruo Kuroda ◽  
Tomofusa Tsuchiya


2009 ◽  
Vol 32 (3) ◽  
pp. 483-488 ◽  
Author(s):  
Toshihiro Nishioka ◽  
Wakano Ogawa ◽  
Teruo Kuroda ◽  
Takashi Katsu ◽  
Tomofusa Tsuchiya


2002 ◽  
Vol 46 (11) ◽  
pp. 3386-3393 ◽  
Author(s):  
Patricia Sánchez ◽  
Ana Alonso ◽  
Jose L. Martinez

ABSTRACT We report on the cloning of the gene smeT, which encodes the transcriptional regulator of the Stenotrophomonas maltophilia efflux pump SmeDEF. SmeT belongs to the TetR and AcrR family of transcriptional regulators. The smeT gene is located upstream from the structural operon of the pump genes smeDEF and is divergently transcribed from those genes. Experiments with S. maltophilia and the heterologous host Escherichia coli have demonstrated that SmeT is a transcriptional repressor. S1 nuclease mapping has demonstrated that expression of smeT is driven by a single promoter lying close to the 5′ end of the gene and that expression of smeDEF is driven by an unique promoter that overlaps with promoter PsmeT. The level of expression of smeT is higher in smeDEF-overproducing S. maltophilia strain D457R, which suggests that SmeT represses its own expression. Band-shifting assays have shown that wild-type strain S. maltophilia D457 contains a cellular factor(s) capable of binding to the intergenic smeT-smeD region. That cellular factor(s) was absent from smeDEF-overproducing S. maltophilia strain D457R. The sequence of smeT from D457R showed a point mutation that led to a Leu166Gln change within the SmeT protein. This change allowed overexpression of both smeDEF and smeT in D457R. It was noteworthy that expression of wild-type SmeT did not fully complement the smeT mutation in D457R. This suggests that the wild-type protein is not dominant over the mutant SmeT.



2008 ◽  
Vol 54 (5) ◽  
pp. 411-416 ◽  
Author(s):  
Sanela Begic ◽  
Elizabeth A. Worobec

Serratia marcescens is an important nosocomial agent having high antibiotic resistance. A major mechanism for S. marcescens antibiotic resistance is active efflux. To ascertain the substrate specificity of the S. marcescens SdeCDE efflux pump, we constructed pump gene deletion mutants. sdeCDE knockout strains showed no change in antibiotic susceptibility in comparison with the parental strains for any of the substrates, with the exception of novobiocin. In addition, novobiocin was the only antibiotic to be accumulated by sdeCDE-deficient strains. Based on the substrates used in our study, we conclude that SdeCDE is a Resistance–Nodulation–Cell Division family pump with limited substrate specificity.



2003 ◽  
Vol 47 (12) ◽  
pp. 937-943 ◽  
Author(s):  
Xing-Jue Xu ◽  
Xian-Zhong Su ◽  
Yuji Morita ◽  
Teruo Kuroda ◽  
Tohru Mizushima ◽  
...  


2003 ◽  
Vol 47 (9) ◽  
pp. 2990-2992 ◽  
Author(s):  
Hiroshi Sekiya ◽  
Takehiko Mima ◽  
Yuji Morita ◽  
Teruo Kuroda ◽  
Tohru Mizushima ◽  
...  

ABSTRACT We isolated mutant YM644, which showed elevated resistance to norfloxacin, ethidium bromide, acriflavine, and rhodamine 6G, from Pseudomonas aeruginosa YM64, a strain that lacks four major multidrug efflux pumps. The genes responsible for the resistance were mexHI-opmD. Elevated ethidium extrusion was observed with cells of YM644 and YM64 harboring a plasmid carrying the genes. Disruption of the genes in the chromosomal DNA of YM644 made the cells sensitive to the drugs.



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