title: Pleiotropic effects of the twin-arginine translocation system on biofilm formation, colonization, and virulence in Vibrio cholerae.
abstract: BACKGROUND
  The Twin-arginine translocation (Tat) system serves to translocate folded proteins, including periplasmic enzymes that bind redox cofactors in bacteria. The Tat system is also a determinant of virulence in some pathogenic bacteria, related to pleiotropic effects including growth, motility, and the secretion of some virulent factors. The contribution of the Tat pathway to Vibrio cholerae has not been explored. Here we investigated the functionality of the Tat system in V. cholerae, the etiologic agent of cholera.
  
  
  RESULTS
  In V. cholerae, the tatABC genes function in the translocation of TMAO reductase. Deletion of the tatABC genes led to a significant decrease in biofilm formation, the ability to attach to HT-29 cells, and the ability to colonize suckling mouse intestines. In addition, we observed a reduction in the output of cholera toxin, which may be due to the decreased transcription level of the toxin gene in tatABC mutants, suggesting an indirect effect of the mutation on toxin production. No obvious differences in flagellum biosynthesis and motility were found between the tatABC mutant and the parental strain, showing a variable effect of Tat in different bacteria.
  
  
  CONCLUSIONS
  The Tat system contributes to the survival of V. cholerae in the environment and in vivo, and it may be associated with its virulence.
authors.affiliation: State Key Laboratory for Infectious Disease Prevention and Control, Department of Diarrheal Diseases, Chinese Center for Disease Control and Prevention, Beijing, PR China. zhanglijuan@icdc.cn
authors.forename: Lijuan
authors.initials: L
authors.lastname: Zhang
authors.forename: Zhaoqin
authors.initials: Z
authors.lastname: Zhu
authors.forename: Huaiqi
authors.initials: H
authors.lastname: Jing
authors.forename: Jingyun
authors.initials: J
authors.lastname: Zhang
authors.forename: Yanwen
authors.initials: Y
authors.lastname: Xiong
authors.forename: Meiying
authors.initials: M
authors.lastname: Yan
authors.forename: Shouyi
authors.initials: S
authors.lastname: Gao
authors.forename: Long-Fei
authors.initials: LF
authors.lastname: Wu
authors.forename: Jianguo
authors.initials: J
authors.lastname: Xu
authors.forename: Biao
authors.initials: B
authors.lastname: Kan
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D018441:Biofilms; D002772:Cholera Toxin / Q000096:biosynthesis*; D005407:Flagella / Q000378:metabolism; D015964:Gene Expression Regulation, Bacterial; D019073:HT29 Cells; D006801:Humans; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D010089:Oxidoreductases, N-Demethylating / Q000378:metabolism; D017384:Sequence Deletion; D014735:Vibrio Infections / Q000382:microbiology; D014734:Vibrio cholerae / Q000235:genetics / Q000254:growth & development* / Q000378:metabolism / Q000472:pathogenicity; D014774:Virulence
chemical_list: D001426:Bacterial Proteins; D026901:Membrane Transport Proteins; D002772:Cholera Toxin; D010089:Oxidoreductases, N-Demethylating; C023186:trimethylamine dehydrogenase