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Transcription of the plasmid‐encoded toxin gene from Enteroaggregative Escherichia coli is regulated by a novel co‐activation mechanism involving CRP and Fis
Author(s) -
Rossiter Amanda E.,
Browning Douglas F.,
Leyton Denisse L.,
Johnson Matthew D.,
Godfrey Rita E.,
Wardius Catherine A.,
Desvaux Mickael,
Cunningham Adam F.,
RuizPerez Fernando,
Nataro James P.,
Busby Stephen J. W.,
Henderson Ian R.
Publication year - 2011
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2011.07685.x
Subject(s) - enteroaggregative escherichia coli , biology , virulence , microbiology and biotechnology , escherichia coli , transcription (linguistics) , plasmid , transposable element , gene , transposon mutagenesis , transcription factor , promoter , mutant , genetics , enterobacteriaceae , gene expression , linguistics , philosophy
Summary Enteroaggregative Escherichia coli (EAEC) is a major cause of diarrhoea in developing countries. EAEC 042 is the prototypical strain. EAEC 042 secretes the functionally well‐characterized Pet autotransporter toxin that contributes to virulence through its cytotoxic effects on intestinal epithelial cells. Following a global transposon mutagenesis screen of EAEC 042, the transcription factors, CRP and Fis, were identified as essential for transcription of the pet gene. Using both in vivo and in vitro techniques, we show that the pet promoter is co‐dependent on CRP and Fis. We present a novel co‐activation mechanism whereby CRP is placed at a non‐optimal position for transcription initiation, creating dependence on Fis for full activation of pet . This study complements previous findings that establish Fis as a key virulence regulator in EAEC 042.