|Lynn, Chan xing m|
Submitted to: Meeting Proceedings
Publication Type: Abstract only
Publication Acceptance Date: 2/11/2004
Publication Date: 5/8/2004
Citation: Bhagwat, A.A., Lynn, C., Shufen, R.H., Moghe, G., Phadke, R., Fernalld, R.T., Cregan, P.B. 2004. Role of response regulatory genes, rpos and gade (formerly yhie) in acid-resistance systems of foodborne outbreak-associated pathogenic escherichia coli strains. In: Proceedings of EURESCO Conference, Bacterial Neural Networks, May 8-14, 2004, San Feliu, Spain, p. 43. Interpretive Summary:
Technical Abstract: The low infection dose of diarrheageneic Escherichia coli strains is attributed to three distinct acid-resistance (AR) systems that have been identified so far. Other than exposure to mild acidic conditions, cessation of growth or environmental stress also induce acid-resistance pathways in E. coli. Expression of the first AR system (AR1 also referred to as oxidative or glucose-repressed system) requires the alternative sigma factor RpoS. This system which protects cells up to pH 3.0, does not require any external amino acid to function. In contrast, AR systems 2 and 3 are amino acid decarboxylase/amtiporter systems that utilize extracellular glutamate (AR2) or arginine (AR3) to protect cells during extreme acid challenges (up to pH 2.0). The glutamate-dependent acid-resistance system (AR2) is believed to be robust and most likely provides the highest protection from stomach acidity. Genetic analysis of AR systems of 82 foodborne outbreak-associated pathogenic E. coli strains (isolated from 34 countries and 23 states within the U.S.A) was carried out. DNA sequencing and heterologous complementation studies revealed occurrence of mutations in rpoS (36% strains) and in the newly discovered LuxR-like regulator GadE (formerly YhiE) (7% strains) genes. In spite of mutations in the rpoS gene, several strains showed acid-resistance by the pathway AR1. Genome-wide expression analysis of AR1 was performed at 5 seconds, 1 min., 3 min., 1 h and 2 h intervals during acid-challenge. The data revealed induction of 158 genes during acid-challenge for AR1 pathway, while de novo protein synthesis was not necessary for pathway AR2.