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Role of hypoxanthine and guanine in regulation of Salmonella typhimurium pur gene expression.

机译:次黄嘌呤和鸟嘌呤在鼠伤寒沙门氏菌pur基因表达调控中的作用。

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Data are presented which indicate that the repression of pur gene expression seen after the addition of preformed purines to cultures of Salmonella typhimurium is the consequence of the presence or the formation of the purine bases, hypoxanthine and guanine. This conclusion is based on the following observations. First, it was impossible to find a correlation between the size of any individual purine nucleotide pool and the level of the first four enzymes in the de novo biosynthetic pathway. Second, adenine plus guanosine served as a perfect source of purine nucleotides, but their presence caused no repression of pur gene expression if the cells lacked purine nucleoside phosphorylase activity. This enzyme is needed to convert adenine and guanosine to hypoxanthine and guanine, but not for their conversion to nucleotides. Third, addition of guanine to a strain lacking guanine phosphoribosyltransferase (gpt) resulted in a repression of the level of the purine de novo biosynthetic enzymes, a reduction of the growth rate, and a fall in the pools of ATP and GTP. Addition of hypoxanthine to a strain lacking hypoxanthine phosphoribosyltransferase (hpt) had a similar, although weaker, effect. If the cells lacked both hypoxanthine and guanine phosphoribosyltransferases (hpt gpt), their basal level of the purine de novo biosynthetic enzymes was repressed in minimal medium. Such cells grow slower than wild-type cells and excrete purines, probably due to the inability to salvage endogenously formed hypoxanthine and guanine.
机译:所提供的数据表明,向鼠伤寒沙门氏菌培养物中加入预先形成的嘌呤后,pur基因表达的抑制是嘌呤碱基,次黄嘌呤和鸟嘌呤存在或形成的结果。该结论基于以下观察。首先,不可能找到任何单个嘌呤核苷酸池的大小与从头生物合成途径中前四种酶的水平之间的相关性。其次,腺嘌呤加鸟嘌呤是嘌呤核苷酸的理想来源,但如果细胞缺乏嘌呤核苷磷酸化酶活性,它们的存在不会抑制pur基因的表达。需要这种酶才能将腺嘌呤和鸟嘌呤转化为次黄嘌呤和鸟嘌呤,但不需要将其转化为核苷酸。第三,向缺乏鸟嘌呤磷酸核糖基转移酶(gpt)的菌株中添加鸟嘌呤导致嘌呤从头生物合成酶的水平降低,生长速率降低以及ATP和GTP库的减少。向缺乏次黄嘌呤磷酸核糖基转移酶(hpt)的菌株添加次黄嘌呤具有相似的作用,尽管作用较弱。如果细胞缺乏次黄嘌呤和鸟嘌呤磷酸核糖基转移酶(hpt gpt),则其嘌呤从头生物合成酶的基础水平将在基本培养基中被抑制。这种细胞的生长速度比野生型细胞和嘌呤嘌呤要慢,这可能是由于无法挽救内源形成的次黄嘌呤和鸟嘌呤所致。

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