Whole genome microarray analysis of the expression profile of Escherichia coli in response to exposure to para-nitrophenol.

Angela Sherry (nee Brown), Jason R. Snape, Colin Harwood, Ian M. Head

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

2 Citations (Scopus)


In ecotoxicology, standard biological assays are used to determine the effects of chemicals on microorganisms. One assay, the microbial multiplication inhibition test, measures the degree of growth inhibition of a population of microorganisms when exposed to a chemical. Whilst this test indicates crude inhibitory effects of chemicals on cells, it offers no insight as to why the cells are inhibited. Genomic array technology was used to investigate the effects of a nitroaromatic compound, para-nitrophenol (PNP), on Escherichia coli K12-MG1655 cells. Global changes in gene expression showed exposure to PNP caused E. coli cells to prematurely enter stationary phase, as shown by downregulation of genes involved in protein synthesis (rpl, rps, rpm). Genes of the emrRAB operon, which confers resistance to compounds that uncouple oxidative phosphorylation, were upregulated in cells in response to PNP exposure. PNP also induced the marRAB operon and dps gene, which bestow resistance to oxidative stress. A compound structurally similar to PNP, dinitrophenol (DNP) a protonophore that uncouples oxidative phosphorylation, has previously been shown to induce the marRAB operon. Like DNP, we suggest that PNP uncouples oxidative phosphorylation within E. coli cells. The upregulated marRAB and emrRAB genes also confer antibiotic resistance and efflux mechanisms, respectively, within E. coli. A downregulation of genes encoding porins, for the transport of solutes, in the outer membrane of cells (ompA, ompC, ompF and ompT), indicated that PNP also affected cell membrane constituents. In addition, rpoE, which encodes a sigma factor involved in cell envelope stress response, was upregulated in cells following PNP exposure. Genes that conferred resistance to low pH (hdeA, hdeB) were upregulated in cells that were exposed to PNP. Furthermore, the acidic nature of the PNP medium may have activated a pH-inducible gene, inaa, which (as with marRAB operon) bestows antibiotic stress resistance in E. coli.
Original languageEnglish
Title of host publicationComparative Toxicogenomics
EditorsC Hogstrand, P Kille
Place of PublicationAmsterdam
Number of pages28
ISBN (Print)9780444532749, 0444532749
Publication statusPublished - 2008
Externally publishedYes

Publication series

NameAdvances in Experimental Biology
ISSN (Print)1872-2423


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