The Translocation and Assembly Module (TAM) of Edwardsiella tarda Is Essential for Stress Resistance and Host Infection
Translocation and assembly module (TAM) is a protein channel known to mediate the secretion of virulence factors during pathogen infection. Edwardsiella tarda is a Gram-negative bacterium that is pathogenic to a wide range of farmed fish and other hosts including humans. In this study, we examined t...
Saved in:
Published in | Frontiers in microbiology Vol. 11; p. 1743 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
24.07.2020
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Translocation and assembly module (TAM) is a protein channel known to mediate the secretion of virulence factors during pathogen infection.
Edwardsiella tarda
is a Gram-negative bacterium that is pathogenic to a wide range of farmed fish and other hosts including humans. In this study, we examined the function of the two components of the TAM, TamA and TamB, of
E. tarda
(named
tamA
Et
and
tamB
Et
, respectively). TamA
Et
was found to localize on the surface of
E. tarda
and be recognizable by TamA
Et
antibody. Compared to the wild type, the
tamA
and
tamB
knockouts, TX01Δ
tamA
and TX01Δ
tamB
, respectively, were significantly reduced in motility, flagella formation, invasion into host cells, intracellular replication, dissemination in host tissues, and inducing host mortality. The lost virulence capacities of TX01Δ
tamA
and TX01Δ
tamB
were restored by complementation with the
tamA
Et
and
tamB
Et
genes, respectively. Furthermore, TX01Δ
tamA
and TX01Δ
tamB
were significantly impaired in the ability to survive under low pH and oxidizing conditions, and were unable to maintain their internal pH balance and cellular structures in acidic environments, which led to increased susceptibility to lysozyme destruction. Taken together, these results indicate that TamA
Et
and TamB
Et
are essential for the virulence of
E. tarda
and required for
E. tarda
to survive under stress conditions. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Lisa Sedger, University of Technology Sydney, Australia This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology Reviewed by: Christopher Stubenrauch, Monash University, Australia; Javier Santander, Memorial University of Newfoundland, Canada |
ISSN: | 1664-302X 1664-302X |
DOI: | 10.3389/fmicb.2020.01743 |