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Repression of heat-stable enterotoxin synthesis in enterotoxigenic Escherichia coli
Author(s) -
J F Alderete,
D C Robertson
Publication year - 1977
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.17.3.629-633.1977
Subject(s) - enterotoxigenic escherichia coli , biology , escherichia coli , heat stable enterotoxin , enterotoxin , glycerol , heat labile enterotoxin , biochemistry , catabolite repression , glycerol kinase , beta galactosidase , microbiology and biotechnology , gene , mutant
Five different carbon sources were examined for their ability to control synthesis of heat-stable enterotoxin (ST) by enterotoxigenic (ENT+) Escherichia coli grown in either a defined medium containing four amino acids or a minimal salts medium. No ST activity was observed when D-glucose, D-gluconate, and L-arabinose were added separately to the defined medium, whereas glycerol and pyruvate decreased toxin levels. Similar results were obtained using a minimal salts medium, except with pyruvate, which did not support growth. Inhibition of ST synthesis by D-glucose was overcome by the addition of 3 X 10(-3) M cyclic adenosine 3',5'-monophosphate. Glucose repression of beta-galactosidase synthesis under conditions optimal for inhibition of ST synthesis was also reversed by exogenous cyclic adenosine 3',5'-monophosphate in the presence of the inducer isopropyl-beta-D-thiogalactopyranoside. The data suggest that control mechanisms for the synthesis of plasmid gene products of bacterial pathogens are similar to those exerted on the host chromosome.

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