Pleiotropic effects of the twin-arginine translocation system on biofilm formation, colonization, and virulence in Vibrio cholerae.
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.
Zhang
Lijuan
L
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
Zhu
Zhaoqin
Z
Jing
Huaiqi
H
Zhang
Jingyun
J
Xiong
Yanwen
Y
Yan
Meiying
M
Gao
Shouyi
S
Wu
Long-Fei
LF
Xu
Jianguo
J
Kan
Biao
B
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
D001426:Bacterial Proteins; D026901:Membrane Transport Proteins; D002772:Cholera Toxin; D010089:Oxidoreductases, N-Demethylating; C023186:trimethylamine dehydrogenase