The bacteria (green) were

immunostained with FITC-labeled antibodies as described in Materials and Methods. HT-29 cells AC220 in vivo (red) were identified by Evan’s blue staining. Discussion In this study, we determined the functionality of the tatABC and tatE genes in V. cholerae. Our study demonstrates that the Tat functions are associated not only with the virulence of V. cholerae but also with its environmental survival. We found that the Tat system is functionally associated with biofilm formation and colonization ability in V. cholerae, and it may indirectly affect the production of cholera toxin. In E. coli, tatABC forms an operon and tatE forms an independent transcriptional unit positioned away from tatABC [4]. Correspondingly, in V. cholerae strain N16961, tatABC is

BIX 1294 clinical trial located in chromosome I, and tatE is located in chromosome II. By searching the GenBank we found the O1 classical biotype strain O395 also possesses tatABC and tatE homologous sequences, we speculate that the toxigenic serogroup O139 strains should also have the tat gene homologue. Whereas further study FHPI manufacturer is needed to confirm the chromosomal distribution of the genes and functions. It is unclear why V. cholerae possesses two chromosomes, perhaps chromosome II plays a specialized independent role under evolutionary selective pressure [19]. It has been observed that several of the regulatory pathways, for regulation in response to both

environmental and pathogenic signals, are divided between the two chromosomes. Also, duplications of genes with at least one of copy of the ORF were found on each chromosome. Most of these genes are involved in V. cholerae biology, notably its ability to inhabit diverse environments [19]. Therefore, the function of tatE in particular should be considered. By using reverse transcription Tolmetin PCR, we found that tatE in chromosome II is also transcribed independently (data not shown). It may not be a simple duplication of tatA in chromosome I because individual deficiency of tatA or tatE still impaired the anaerobic growth of mutants in M9-TMAO media in comparison to the wild type strain. Biofilm formation is crucial for the survival of V. cholerae under environmental stress. The formation of biofilm can also make V. cholerae more resistant to acidic environments and increase its ability to break through the gastric acid barrier in humans [38]. In this study, we noticed that biofilm formation in the tatABC mutant was impaired, but it could be restored by complementation with functional tatABC genes. In P. aeruginosa [11] and E. coli [39], biofilm formation of the tatC mutants is also defective. It has been shown that the failure to form biofilms in the E. coli tatC mutant strain is due to defects in the cell envelope [39].