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SOS regulation of the type III secretion system of enteropathogenic Escherichia coli.

SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Research Abstract Details 

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  • SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Abstract Text:

    jay l melliesJay L Mellies,kenneth r haackKenneth R Haack,derek c galliganDerek C Galligan,

    Genomes of bacterial pathogens contain and coordinately regulate virulence-associated genes in order to cause disease. Enteropathogenic Escherichia coli (EPEC), a major cause of watery diarrhea in infants and a model gram-negative pathogen, expresses a type III secretion system (TTSS) that is encoded by the locus of enterocyte effacement (LEE) and is necessary for causing attaching and effacing intestinal lesions. Effector proteins encoded by the LEE and in cryptic prophage are injected into the host cell cytoplasm by the TTTS apparatus, ultimately leading to diarrhea. The LEE is comprised of multiple polycistronic operons, most of which are controlled by the global, positive regulator Ler. Here we demonstrated that the LEE2 and LEE3 operons also responded to SOS signaling and that this regulation was LexA dependent. As determined by a DNase I protection assay, purified LexA protein bound in vitro to a predicted SOS box located in the divergent, overlapping LEE2/LEE3 promoters. Expression of the lexA1 allele, encoding an uncleavable LexA protein in EPEC, resulted in reduced secretion, particularly in the absence of the Ler regulator. Finally, we obtained evidence that the cryptic phage-located nleA gene encoding an effector molecule is SOS regulated. Thus, we demonstrated, for the first time to our knowledge, that genes encoding components of a TTSS are regulated by the SOS response, and our data might explain how a subset of EPEC effector proteins, encoded in cryptic prophages, are coordinately regulated with the LEE-encoded TTSS necessary for their translocation into host cells.

    SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Publishing Authors By Initials

    jl melliesJL Mellies,kr haackKR Haack,dc galliganDC Galligan,

    For similar enzymes and coenzymes: enzymes: hydrolases: peptide hydrolases: endopeptidases: serine endopeptidases research abstracts see: enzymes and coenzymes: enzymes: hydrolases: peptide hydrolases: endopeptidases: serine endopeptidases research

    PUBMED ID PMID:

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    SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Journal of bacteriology

    VOLUME: 189

    Page Numbers: 2863-72

    Journal Abbreviation: J. Bacteriol.

    ISSN: 0021-9193

    DAY: 19

    MONTH: 01

    YEAR: 2007

    SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985120

    SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Keywords Mesh Terms:

    KEYWORDS: Serine Endopeptidases

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: SOS regulation of the type III secretion system of enteropathogenic Escherichia coli. Information

    Substance Name: Serine Endopeptidases

    Registry Number: EC 3.4.21.-

    Grant and Affiliation Information for SOS regulation of the type III secretion system of enteropathogenic Escherichia coli.

    AFFILIATION: Biology Department, Reed College, 3203 S.E. Woodstock Blvd., Portland, OR 97202, USA. jay.mellies@reed.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: R15 AI047802-02

    ACRONYM: AI

    MEDLINETA: J Bacteriol

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