The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli

The twin-arginine translocation (Tat) system is involved in a variety of important bacterial physiological processes. Conserved among bacteria and crucial for virulence, the Tat system is deemed as a promising anti-microbial drug target. However, the mechanism of how the Tat system functions in bact...

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Autores principales: Jinjin Liu, Fan Yin, Te Liu, Shaowen Li, Chen Tan, Lu Li, Rui Zhou, Qi Huang
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Lenguaje:EN
Publicado: Taylor & Francis Group 2020
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spelling oai:doaj.org-article:96875125b71b4e4391e2b70672fd02e32021-11-17T14:21:59ZThe Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli2150-55942150-560810.1080/21505594.2020.1817709https://doaj.org/article/96875125b71b4e4391e2b70672fd02e32020-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2020.1817709https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608The twin-arginine translocation (Tat) system is involved in a variety of important bacterial physiological processes. Conserved among bacteria and crucial for virulence, the Tat system is deemed as a promising anti-microbial drug target. However, the mechanism of how the Tat system functions in bacterial pathogenesis has not been fully understood. In this study, we showed that the Tat system was critical for the virulence of an extra-intestinal pathogenic E. coli (ExPEC) strain PCN033. A total of 20 Tat-related mutant strains were constructed, and competitive infection assays were performed to evaluate the relative virulence of these mutants. The results demonstrated that several Tat substrate mutants, including the ΔsufI, ΔamiAΔamiC double mutant as well as each single mutant, ΔyahJ, ΔcueO, and ΔnapG, were significantly outcompeted by the WT strain, among which the ΔsufI and ΔamiAΔamiC strains showed the lowest competitive index (CI) value. Results of individual mouse infection assay, in vitro cell adhesion assay, whole blood bactericidal assay, and serum bactericidal assay further confirmed the virulence attenuation phenotype of the ΔsufI and ΔamiAΔamiC strains. Moreover, the two mutants displayed chained morphology in the log phase resembling the Δtat and were defective in stress response. Our results suggest that the Tat system and its dependent cell division proteins SufI, AmiA, and AmiC play critical roles during ExPEC pathogenesis.Jinjin LiuFan YinTe LiuShaowen LiChen TanLu LiRui ZhouQi HuangTaylor & Francis Grouparticletwin-arginine protein translocation (tat) systemextra-intestinal pathogenic escherichia coli (expec)tat substrate proteincell divisionstress responsepathogenesisInfectious and parasitic diseasesRC109-216ENVirulence, Vol 11, Iss 1, Pp 1279-1292 (2020)
institution DOAJ
collection DOAJ
language EN
topic twin-arginine protein translocation (tat) system
extra-intestinal pathogenic escherichia coli (expec)
tat substrate protein
cell division
stress response
pathogenesis
Infectious and parasitic diseases
RC109-216
spellingShingle twin-arginine protein translocation (tat) system
extra-intestinal pathogenic escherichia coli (expec)
tat substrate protein
cell division
stress response
pathogenesis
Infectious and parasitic diseases
RC109-216
Jinjin Liu
Fan Yin
Te Liu
Shaowen Li
Chen Tan
Lu Li
Rui Zhou
Qi Huang
The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
description The twin-arginine translocation (Tat) system is involved in a variety of important bacterial physiological processes. Conserved among bacteria and crucial for virulence, the Tat system is deemed as a promising anti-microbial drug target. However, the mechanism of how the Tat system functions in bacterial pathogenesis has not been fully understood. In this study, we showed that the Tat system was critical for the virulence of an extra-intestinal pathogenic E. coli (ExPEC) strain PCN033. A total of 20 Tat-related mutant strains were constructed, and competitive infection assays were performed to evaluate the relative virulence of these mutants. The results demonstrated that several Tat substrate mutants, including the ΔsufI, ΔamiAΔamiC double mutant as well as each single mutant, ΔyahJ, ΔcueO, and ΔnapG, were significantly outcompeted by the WT strain, among which the ΔsufI and ΔamiAΔamiC strains showed the lowest competitive index (CI) value. Results of individual mouse infection assay, in vitro cell adhesion assay, whole blood bactericidal assay, and serum bactericidal assay further confirmed the virulence attenuation phenotype of the ΔsufI and ΔamiAΔamiC strains. Moreover, the two mutants displayed chained morphology in the log phase resembling the Δtat and were defective in stress response. Our results suggest that the Tat system and its dependent cell division proteins SufI, AmiA, and AmiC play critical roles during ExPEC pathogenesis.
format article
author Jinjin Liu
Fan Yin
Te Liu
Shaowen Li
Chen Tan
Lu Li
Rui Zhou
Qi Huang
author_facet Jinjin Liu
Fan Yin
Te Liu
Shaowen Li
Chen Tan
Lu Li
Rui Zhou
Qi Huang
author_sort Jinjin Liu
title The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
title_short The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
title_full The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
title_fullStr The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
title_full_unstemmed The Tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic Escherichia coli
title_sort tat system and its dependent cell division proteins are critical for virulence of extra-intestinal pathogenic escherichia coli
publisher Taylor & Francis Group
publishDate 2020
url https://doaj.org/article/96875125b71b4e4391e2b70672fd02e3
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