Mickael, C. S., Lam, P.-K. S., Berberov, E. M., Allan, B., Potter, A. A., Koster, W.
Salmonella enterica subsp. enterica serovar Enteritidis is a leading causative agent of gastroenteritis in humans. This pathogen also colonizes the intestinal tracts of poultry and can spread systemically in chickens. Transfer to humans usually occurs through undercooked or improperly handled poultry meat or eggs. The bacterial twin-arginine transport (Tat) pathway is responsible for the translocation of folded proteins across the cytoplasmic membrane. In order to study the role of the Tat system in the infection and colonization of chickens by Salmonella Enteritidis, we constructed chromosomal deletion mutants of the tatB and tatC genes, which are essential components of the Tat translocon. We observed that the tat mutations affected bacterial cell morphology, motility, and sensitivity to albomycin, sodium dodecyl sulfate (SDS), and EDTA. In addition, the mutant strains showed reduced invasion of polarized Caco-2 cells. The wild-type phenotype was restored in all our Salmonella Enteritidis tat mutants by introducing episomal copies of the tatABC genes. When tested in chickens by use of a Salmonella Enteritidis tatB strain, the Tat system inactivation did not substantially affect cecal colonization, but it delayed systemic infection. Taken together, our data demonstrated that the Tat system plays a role in Salmonella Enteritidis pathogenesis.
Very interesting paper. Tat has been implicated as an important factor in many pathogenic bacteria- as one might expect for a major secretion system. Perhaps these mutants ability to invade is affected by their reduced motility. Do equivalent numbers of WT and tat mutants reach the Caco-2 monolayer?
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A interesting paper, the authors characterized the conservative two-arginine transport pathway, TAT system, in Salmonella, particularly investigated the virulence role of TAT system in Chickens.
It will be nicer for the authors to illustrate more about the pathogenic or virulence connection of those perturbation being investigated in the paper, such as, SDS, EDTA and albomycin, in addition to recapitulate the function of TAT system in E.coli, because, the substrates between E.coli and Salmonella for TAT system may or may not be the same, though the genes share high conservation.
The paper showed clearly different Salmonella infection consequence between day 4 postchallenge for chickens at age of 4 days and day 1 postchallenge for chickens at age of 7 days, notably, the chickens were all about at age of 8 days. Probably, this is some thing that should be kept in mind when doing Chicken experiments, ie, it seems some kind of fundamental difference between chickens at the age of 4 days and 7 days in term to the susceptibility of Salmonella.
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I think all of the phenotypes may be explained by the reduced cell separation resulting from the reduced amidase activity. Reduced cell separation will result in increased outer membrane permeability and increased sensitivity to a variety of agents. The researchers might be able to tease apart the amidase effects from those of other Tat-transported proteins by increasing expression of AmiB.
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Authors well characterized Salmonella Enteritidis tatB and tatC mutants by cell morphology, motility, curli expression, EDTA, SDS sensitivity, antibiotic resistant and invasion assay. However the mechanism/Function of Tat system in Salmonella is still not clear. It may or not the same as in E.coli. Regarding chicken experiment I’m curious that why different age of chick showed different results. Is it nothing related with immune responses?
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