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磷酸烯醇式丙酮酸:糖磷酸转移酶系统介导的鼠伤寒沙门氏菌碳水化合物代谢调控

Phosphoenolpyruvate:sugar phosphotransferase system-mediated regulation of carbohydrate metabolism in Salmonella typhimurium.

作者信息

Nelson S O, Scholte B J, Postma P W

出版信息

J Bacteriol. 1982 May;150(2):604-15. doi: 10.1128/jb.150.2.604-615.1982.

Abstract

The crr mutation was shown to affect the phosphoenolpyruvate:sugar phosphotransferase system-mediated transient repression of the lac operon, intracellular cAMP levels, and sensitivity to inducer exclusion. Our results indicate that the presumed crr gene product, factor IIIGlc, plays a direct role in the regulation of inducer exclusion. We propose a mechanism in which inducer exclusion depends on both the level and state of phosphorylation of factor IIIGlc and the level of an inducer exclusion-sensitive transport system. The results of studies on the sensitivity to inducer exclusion of glycerol and maltose in cultures induced for short periods of time on these substrates (resulting in varying degrees of activity of the respective transport systems) support this model of inducer exclusion. Previously, the crp*-771 mutation has been shown to result in an altered cAMP receptor protein, which has a changed affinity for cAMP, and to affect the sensitivity for inducer exclusion of glycerol. Changes in other functions of the altered cAMP receptor protein were indicated by our results; these changes were in the roles of this protein in (i) the cAMP-dependent initiation of transcription of the lac operon and (ii) the regulation of intracellular cAMP levels and the export of cAMP. We propose that the crp*-771 mutation has an indirect effect in relieving inducer exclusion in repressed or hypersensitive strains, in which the crp*-771 mutation allows the synthesis of inducer exclusion-sensitive transport systems to higher levels than the levels found in strains containing wild-type cAMP receptor protein.

摘要

crr突变被证明会影响磷酸烯醇丙酮酸:糖磷酸转移酶系统介导的乳糖操纵子的瞬时抑制、细胞内cAMP水平以及对诱导物排除的敏感性。我们的结果表明,推测的crr基因产物因子IIIGlc在诱导物排除的调节中起直接作用。我们提出了一种机制,其中诱导物排除取决于因子IIIGlc的磷酸化水平和状态以及诱导物排除敏感转运系统的水平。对在这些底物上短时间诱导培养的甘油和麦芽糖对诱导物排除敏感性的研究结果(导致各自转运系统的活性程度不同)支持了这种诱导物排除模型。以前,crp*-771突变已被证明会导致cAMP受体蛋白发生改变,其对cAMP的亲和力发生变化,并影响甘油对诱导物排除的敏感性。我们的结果表明了改变的cAMP受体蛋白的其他功能变化;这些变化体现在该蛋白在(i)乳糖操纵子转录的cAMP依赖性起始和(ii)细胞内cAMP水平调节及cAMP输出中的作用。我们提出,crp*-771突变在缓解受抑制或超敏感菌株中的诱导物排除方面具有间接作用,其中crp*-771突变允许诱导物排除敏感转运系统合成到比含有野生型cAMP受体蛋白的菌株中更高的水平。

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