Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains

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@article{1576a52f9a5441d0a39d0e53137bc9d0,
title = "Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains",
abstract = "The type III protein secretion system is an important pathogenicity factor of enteropathogenic and enterohaemorrhagic Escherichia coli pathotypes. The genes encoding this apparatus are located on a pathogenicity island (the locus of enterocyte effacement) and are transcriptionally activated by the master regulator Ler. In each pathotype Ler is also known to regulate genes located elsewhere on the chromosome, but the full extent of the Ler regulon is unclear, especially for enteropathogenic E. coli. The Ler regulon was defined for two strains of E. coli: E2348/69 (enteropathogenic) and EDL933 (enterohaemorrhagic) in mid and late log phases of growth by DNA microarray analysis of the transcriptomes of wild-type and ler mutant versions of each strain. In both strains the Ler regulon is focused on the locus of enterocyte effacement - all major transcriptional units of which are activated by Ler, with the sole exception of the LEE1 operon during mid-log phase growth in E2348/69. However, the Ler regulon does extend more widely and also includes unlinked pathogenicity genes: in E2348/69 more than 50 genes outside of this locus were regulated, including a number of known or potential pathogenicity determinants; in EDL933 only 4 extra-LEE genes, again including known pathogenicity factors, were activated. In E2348/69, where the Ler regulon is clearly growth phase dependent, a number of genes including the plasmid-encoded regulator operon perABC, were found to be negatively regulated by Ler. Negative regulation by Ler of PerC, itself a positive regulator of the ler promoter, suggests a negative feedback loop involving these proteins.",
keywords = "Adaptation, Physiological, Enterohemorrhagic Escherichia coli, Enteropathogenic Escherichia coli, Escherichia coli Proteins, Evolution, Molecular, Gene Transfer, Horizontal, Genome, Bacterial, Oligonucleotide Array Sequence Analysis, Regulon, Trans-Activators, Transcription, Genetic",
author = "Lewis Bingle and Chrystala Constantinidou and Shaw, {Robert K} and Islam, {Md Shahidul} and Mala Patel and Snyder, {Lori A S} and Lee, {David J} and Penn, {Charles W} and Busby, {Stephen J W} and Pallen, {Mark J}",
year = "2014",
month = jan,
day = "14",
doi = "10.1371/journal.pone.0080160",
language = "English",
volume = "9",
journal = "PLoSONE",
issn = "1932-6203",
publisher = "Public Library of Science (PLOS)",
number = "1",

}

RIS

TY - JOUR

T1 - Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains

AU - Bingle, Lewis

AU - Constantinidou, Chrystala

AU - Shaw, Robert K

AU - Islam, Md Shahidul

AU - Patel, Mala

AU - Snyder, Lori A S

AU - Lee, David J

AU - Penn, Charles W

AU - Busby, Stephen J W

AU - Pallen, Mark J

PY - 2014/1/14

Y1 - 2014/1/14

N2 - The type III protein secretion system is an important pathogenicity factor of enteropathogenic and enterohaemorrhagic Escherichia coli pathotypes. The genes encoding this apparatus are located on a pathogenicity island (the locus of enterocyte effacement) and are transcriptionally activated by the master regulator Ler. In each pathotype Ler is also known to regulate genes located elsewhere on the chromosome, but the full extent of the Ler regulon is unclear, especially for enteropathogenic E. coli. The Ler regulon was defined for two strains of E. coli: E2348/69 (enteropathogenic) and EDL933 (enterohaemorrhagic) in mid and late log phases of growth by DNA microarray analysis of the transcriptomes of wild-type and ler mutant versions of each strain. In both strains the Ler regulon is focused on the locus of enterocyte effacement - all major transcriptional units of which are activated by Ler, with the sole exception of the LEE1 operon during mid-log phase growth in E2348/69. However, the Ler regulon does extend more widely and also includes unlinked pathogenicity genes: in E2348/69 more than 50 genes outside of this locus were regulated, including a number of known or potential pathogenicity determinants; in EDL933 only 4 extra-LEE genes, again including known pathogenicity factors, were activated. In E2348/69, where the Ler regulon is clearly growth phase dependent, a number of genes including the plasmid-encoded regulator operon perABC, were found to be negatively regulated by Ler. Negative regulation by Ler of PerC, itself a positive regulator of the ler promoter, suggests a negative feedback loop involving these proteins.

AB - The type III protein secretion system is an important pathogenicity factor of enteropathogenic and enterohaemorrhagic Escherichia coli pathotypes. The genes encoding this apparatus are located on a pathogenicity island (the locus of enterocyte effacement) and are transcriptionally activated by the master regulator Ler. In each pathotype Ler is also known to regulate genes located elsewhere on the chromosome, but the full extent of the Ler regulon is unclear, especially for enteropathogenic E. coli. The Ler regulon was defined for two strains of E. coli: E2348/69 (enteropathogenic) and EDL933 (enterohaemorrhagic) in mid and late log phases of growth by DNA microarray analysis of the transcriptomes of wild-type and ler mutant versions of each strain. In both strains the Ler regulon is focused on the locus of enterocyte effacement - all major transcriptional units of which are activated by Ler, with the sole exception of the LEE1 operon during mid-log phase growth in E2348/69. However, the Ler regulon does extend more widely and also includes unlinked pathogenicity genes: in E2348/69 more than 50 genes outside of this locus were regulated, including a number of known or potential pathogenicity determinants; in EDL933 only 4 extra-LEE genes, again including known pathogenicity factors, were activated. In E2348/69, where the Ler regulon is clearly growth phase dependent, a number of genes including the plasmid-encoded regulator operon perABC, were found to be negatively regulated by Ler. Negative regulation by Ler of PerC, itself a positive regulator of the ler promoter, suggests a negative feedback loop involving these proteins.

KW - Adaptation, Physiological

KW - Enterohemorrhagic Escherichia coli

KW - Enteropathogenic Escherichia coli

KW - Escherichia coli Proteins

KW - Evolution, Molecular

KW - Gene Transfer, Horizontal

KW - Genome, Bacterial

KW - Oligonucleotide Array Sequence Analysis

KW - Regulon

KW - Trans-Activators

KW - Transcription, Genetic

U2 - 10.1371/journal.pone.0080160

DO - 10.1371/journal.pone.0080160

M3 - Article

C2 - 24454682

VL - 9

JO - PLoSONE

JF - PLoSONE

SN - 1932-6203

IS - 1

M1 - e80160

ER -