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产肠毒素大肠杆菌中热稳定肠毒素合成的抑制

Repression of heat-stable enterotoxin synthesis in enterotoxigenic Escherichia coli.

作者信息

Alderete J F, Robertson D C

出版信息

Infect Immun. 1977 Sep;17(3):629-33. doi: 10.1128/iai.17.3.629-633.1977.

Abstract

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.

摘要

研究了五种不同碳源对产肠毒素(ENT+)大肠杆菌在含有四种氨基酸的限定培养基或基本盐培养基中生长时热稳定肠毒素(ST)合成的控制能力。当将D-葡萄糖、D-葡萄糖酸盐和L-阿拉伯糖分别添加到限定培养基中时,未观察到ST活性,而甘油和丙酮酸可降低毒素水平。使用基本盐培养基也得到了类似结果,但丙酮酸不支持生长。添加3×10⁻³M环腺苷3',5'-单磷酸可克服D-葡萄糖对ST合成的抑制作用。在抑制ST合成的最佳条件下,外源性环腺苷3',5'-单磷酸在诱导剂异丙基-β-D-硫代半乳糖苷存在时,也可逆转葡萄糖对β-半乳糖苷酶合成的阻遏作用。数据表明,细菌病原体质粒基因产物合成的控制机制与宿主染色体上的控制机制相似。

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