Cargando…

AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection

Bacteria can change its lifestyle during inhabiting in host niches where they survive and replicate by rapidly altering gene expression pattern to accommodate the new environment. In this study, two novel regulators in avian pathogenic Escherichia coli (APEC) were identified and designated as AutA a...

Descripción completa

Detalles Bibliográficos
Autores principales: Zhuge, Xiangkai, Tang, Fang, Zhu, Hongfei, Mao, Xiang, Wang, Shaohui, Wu, Zongfu, Lu, Chengping, Dai, Jianjun, Fan, Hongjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844996/
https://www.ncbi.nlm.nih.gov/pubmed/27113849
http://dx.doi.org/10.1038/srep25085
_version_ 1782428859201748992
author Zhuge, Xiangkai
Tang, Fang
Zhu, Hongfei
Mao, Xiang
Wang, Shaohui
Wu, Zongfu
Lu, Chengping
Dai, Jianjun
Fan, Hongjie
author_facet Zhuge, Xiangkai
Tang, Fang
Zhu, Hongfei
Mao, Xiang
Wang, Shaohui
Wu, Zongfu
Lu, Chengping
Dai, Jianjun
Fan, Hongjie
author_sort Zhuge, Xiangkai
collection PubMed
description Bacteria can change its lifestyle during inhabiting in host niches where they survive and replicate by rapidly altering gene expression pattern to accommodate the new environment. In this study, two novel regulators in avian pathogenic Escherichia coli (APEC) were identified and designated as AutA and AutR. RT-PCR and β-galactosidase assay results showed that AutA and AutR co-regulated the expression of adhesin UpaB in APEC strain DE205B. Electrophoretic mobility shift assay showed that AutA and AutR could directly bind the upaB promoter DNA. In vitro transcription assay indicated that AutA could activate the upaB transcription, while AutR inhibited the upaB transcription due to directly suppressing the activating effect of AutA on UpaB expression. Transcriptome analysis showed that AutA and AutR coherently affected the expression of hundreds of genes. Our study confirmed that AutA and AutR co-regulated the expression of DE205B K1 capsule and acid resistance systems in E. coli acid fitness island (AFI). Moreover, phenotypic heterogeneity in expression of K1 capsule and acid resistance systems in AFI during host–pathogen interaction was associated with the regulation of AutA and AutR. Collectively speaking, our studies presented that AutA and AutR are involved in APEC adaptive lifestyle change to facilitate its infection.
format Online
Article
Text
id pubmed-4844996
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Nature Publishing Group
record_format MEDLINE/PubMed
spelling pubmed-48449962016-04-29 AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection Zhuge, Xiangkai Tang, Fang Zhu, Hongfei Mao, Xiang Wang, Shaohui Wu, Zongfu Lu, Chengping Dai, Jianjun Fan, Hongjie Sci Rep Article Bacteria can change its lifestyle during inhabiting in host niches where they survive and replicate by rapidly altering gene expression pattern to accommodate the new environment. In this study, two novel regulators in avian pathogenic Escherichia coli (APEC) were identified and designated as AutA and AutR. RT-PCR and β-galactosidase assay results showed that AutA and AutR co-regulated the expression of adhesin UpaB in APEC strain DE205B. Electrophoretic mobility shift assay showed that AutA and AutR could directly bind the upaB promoter DNA. In vitro transcription assay indicated that AutA could activate the upaB transcription, while AutR inhibited the upaB transcription due to directly suppressing the activating effect of AutA on UpaB expression. Transcriptome analysis showed that AutA and AutR coherently affected the expression of hundreds of genes. Our study confirmed that AutA and AutR co-regulated the expression of DE205B K1 capsule and acid resistance systems in E. coli acid fitness island (AFI). Moreover, phenotypic heterogeneity in expression of K1 capsule and acid resistance systems in AFI during host–pathogen interaction was associated with the regulation of AutA and AutR. Collectively speaking, our studies presented that AutA and AutR are involved in APEC adaptive lifestyle change to facilitate its infection. Nature Publishing Group 2016-04-26 /pmc/articles/PMC4844996/ /pubmed/27113849 http://dx.doi.org/10.1038/srep25085 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Zhuge, Xiangkai
Tang, Fang
Zhu, Hongfei
Mao, Xiang
Wang, Shaohui
Wu, Zongfu
Lu, Chengping
Dai, Jianjun
Fan, Hongjie
AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title_full AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title_fullStr AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title_full_unstemmed AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title_short AutA and AutR, Two Novel Global Transcriptional Regulators, Facilitate Avian Pathogenic Escherichia coli Infection
title_sort auta and autr, two novel global transcriptional regulators, facilitate avian pathogenic escherichia coli infection
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844996/
https://www.ncbi.nlm.nih.gov/pubmed/27113849
http://dx.doi.org/10.1038/srep25085
work_keys_str_mv AT zhugexiangkai autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT tangfang autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT zhuhongfei autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT maoxiang autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT wangshaohui autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT wuzongfu autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT luchengping autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT daijianjun autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection
AT fanhongjie autaandautrtwonovelglobaltranscriptionalregulatorsfacilitateavianpathogenicescherichiacoliinfection