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ppGpp with DksA controls gene expression in the locus of enterocyte effacement (LEE) pathogenicity island of enterohaemorrhagic Escherichia coli through activation of two virulence regulatory genes
Author(s) -
Nakanishi Noriko,
Abe Hiroyuki,
Ogura Yoshitoshi,
Hayashi Tetsuya,
Tashiro Kosuke,
Kuhara Satoru,
Sugimoto Nakaba,
Tobe Toru
Publication year - 2006
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.1365-2958.2006.05217.x
Subject(s) - biology , stringent response , pathogenicity island , virulence , gene , escherichia coli , regulation of gene expression , transcription (linguistics) , rna polymerase , gene expression , genetics , sigma factor , locus (genetics) , microbiology and biotechnology , linguistics , philosophy
Summary For a new pathogen to emerge, it must acquire both virulence genes and a system for responding to changes in environmental conditions. Starvation of nutrients or growth arrest induces the stringent response in Escherichia coli , via increased ppGpp. We found the adherence capacity of enterohaemorrhagic E. coli (EHEC) and gene expression in the locus of enterocyte effacement (LEE) were enhanced by a downshift in nutrients or by entry into the stationary growth phase, both of which increase the ppGpp concentration. The activation was dependent on relA and spoT , which encode enzymes for the synthesis and degradation of ppGpp, and on dksA , which encodes an RNA polymerase accessory protein required for the stringent response. Upon induction of RelA expression, LEE gene transcription was activated within 20 min, even without starvation. The expression of two LEE transcriptional regulators, Ler and Pch, was activated by ppGpp and essential for the enhancement of LEE gene expression. In addition, the ler and pch promoters were directly activated by ppGpp in an in vitro transcription system. These findings suggest that the regulation of virulence genes in EHEC is integrated with E. coli 's stringent response system, through the regulation of virulence regulatory genes.