• Title/Summary/Keyword: luxS mutation

Search Result 4, Processing Time 0.018 seconds

Omics-Based Analysis of the luxS Mutation in a Clinical Isolate of Escherichia coli O157:H7 in Korea

  • Kim, Jong-Chul;Yoon, Jang-Won;Kim, Jong-Bae;Oh, Kyung-Hwan;Park, Mi-Sun;Lee, Bok-Kwon;Cho, Seung-Hak
    • Journal of Microbiology and Biotechnology
    • /
    • v.20 no.2
    • /
    • pp.415-424
    • /
    • 2010
  • The purpose of this study was to investigate the relationship between the global regulatory mechanism known as quorum sensing and expression of virulence factors in Escherichia coli O157:87. A nonpolar luxS deletion was introduced into the chromosome of strain CI03J, a human clinical isolate from South Korea, to create the ${\Delta}luxS$ mutant strain ML03J. Phenotypic characterization of wild-type and mutant strains demonstrated that ML03J had no obvious growth or metabolic defects on 0.2% glucose LB medium, produced a functionally defective flagellum, and could not utilize sorbose; the biological significance of sorbose utilization is unknown. Omics-based analysis revealed the involvement of LuxS in the transcriptional activation of several flagella/chemotaxisrelated genes (flhD; fliA, C, D, S, Z; and cheA, Y, Z), repression of glutamate-dependent acid resistance genes (gadAB), and expression of virulence factors including Shiga toxin, hemolysin, and SepD within the LEE pathogenicity island.

luxS and smcR Quorum-Sensing System of Vibrio vulnificus as an Important Factor for In Vivo Survival

  • SHIN NA-RI;BAEK CHANG-HO;LEE DEOG-YONG;CHO YOUNG-WOOK;PARK DAE-KYUN;LEE KO-EUN;KIM KUN-SOO;YOO HAN-SANG
    • Journal of Microbiology and Biotechnology
    • /
    • v.15 no.6
    • /
    • pp.1197-1206
    • /
    • 2005
  • Vibrio vulnificus is an opportunistic pathogen that causes a septicemia and expresses numerous virulence factors, in which luxS and smcR are genes encoding for components responsible for quorum-sensing regulation. In the present study, null mutants were constructed with lesions in each or both of these two genes from the V. vulnificus Vv$\Delta$Z strain, which is a lacZ$^{-}$ and chloramphenicol/streptomycin-resistant derivative of the wild-type ATCC29307 strain, and their phenotypes related to virulence were compared with those of the parental cells. $LD_{50}$ and histopathological findings of luxS-, smcR-, or luxS- smcR- deficient mutant were not different from those of the parent strain, a lacZ-deficient streptomycin-resistant strain in mice. However, time of death in mice was delayed, and numbers of bacteria survived in bloodstream after intraperitoneal injection in mice were decreased by mutation, especially luxS and smcR double mutant (VvSR$\Delta$ZSR). These phenomena were supported by increased serum sensitivity and delayed bacterial proliferation in both murine blood and iron-restricted medium. These results suggest that the luxS and luxR homologous genes in V. vulnificus could playa role in bacterial survival in host by enhancing proliferation and adjusting to changed environment.

Interaction Between the Quorum Sensing and Stringent Response Regulation Systems in the Enterohemorrhagic Escherichia coli O157:H7 EDL933 Strain

  • Oh, Kyung-Hwan;Cho, Seung-Hak
    • Journal of Microbiology and Biotechnology
    • /
    • v.24 no.3
    • /
    • pp.401-407
    • /
    • 2014
  • Quorum sensing and the stringent response are well-known regulation systems for the expression of virulence genes in enterohemorrhagic Escherichia coli (EHEC). However, how these two systems interact is not well known. E. coli strains with mutations in two regulation systems, ${\Delta}luxS$ (ECM101) and ${\Delta}luxS{\Delta}relA{\Delta}spoT$ (ECM201), and the ${\Delta}luxS$ complement strain to ECM201 (ECM202) were created from EHEC O157:H7 EDL933 to investigate how the regulatory systems interact. The phenotypic changes of the mutant strains were characterized and compared with the wild type. The mutant strains exhibited no obvious growth defects, although acid resistance and cellular cytotoxicity were decreased significantly in all the mutant strains. Phenotypic characterization revealed that mutations in the stringent response system (ECM201 and ECM202) influenced the metabolic (defective utilization of arabinose and L-sorbose) and enzymatic activities (decreased trypsin activity, and increased ${\alpha}$-glucosidase activity). In contrast, the quorum sensing system mutant (ECM101) did not display these phenotypes. The motility of the quorum sensing system mutant (ECM101) was unchanged, but mutation in the stringent response system influenced the motility. Our results suggest that quorum sensing interacts with the stringent response regulation system.

Positive Regulation of Pyoluteorin Biosynthesis in Pseudomonas sp. M18 by Quorum-Sensing Regulator VqsR

  • Huang, Xianqing;Zhang, Xuehong;Xu, Yuquan
    • Journal of Microbiology and Biotechnology
    • /
    • v.18 no.5
    • /
    • pp.828-836
    • /
    • 2008
  • The biocontrol rhizobacterium Pseudomonas sp. M18 can produce two kinds of antibiotics, namely pyoluteorin (Plt) and phenazine-1-carboxylic acid (PCA), and is antagonistic against a number of soilborne phytopathogens. In this study, a luxR-type quorum-sensing regulatory gene, vqsR, was identified and characterized immediately downstream of the Plt gene cluster in strain MI8. A vqsR-inactivated mutant led to a significant decrease in the production of Plt and its biosynthetic gene expression. However, this was restored when introducing the vqsR gene by cloning into the plasmid pME6032 in trans. The vqsR mutation did not exert any obvious influence on the production of PCA and its biosynthetic gene expression and the production of N-acylhomoserine lactones (C4 and C8-HSLs) and their biosynthetic gene rhlI expression. Accordingly, these results introduce VqsR as a regulator of Plt production in Pseudomonas spp., and suggest that the regulatory mechanism of vqsR in strain M18 is distinct from that in P. aeruginosa. In addition, it was demonstrated that vqsR mutation did not have any obvious impact on the expression of Plt-specific ABC transporters and other secondary metabolic global regulators, including GacA, RpoS, and RsmA.