Shioi J I, Galloway R J, Niwano M, Chinnock R E, Taylor B L
J Biol Chem. 1982 Jul 25;257(14):7969-75.
Evidence is presented that chemotaxis requires ATP or a closely related metabolite, in addition to its known requirements of ATP for synthesis of S-adenosylmethionine (AdoMet) and maintenance of the proton motive force. Previous studies demonstrated a loss of tumbling and chemotaxis, and depletion of ATP when hisF auxotrophs of Salmonella typhimurium are starved for histidine (Galloway, R. J., and Taylor, B. L. (1980) J. Bacteriol. 144, 1068-1075). In the present study, intracellular [AdoMet], membrane potential, and [ATP] were measured in a hisF mutant of S. typhimurium. Membrane potential, determined from partitioning of [3H]tetraphenylphosphonium ion between the inside and the outside of the cell, was about -150 mV at pH 7.6, and did not decrease in histidine starvation but was slightly increased. The concentration of AdoMet decreased from 0.4 mM to 0.3 mM during starvation but when cycloleucine, an inhibitor of AdoMet synthetase, was used to decrease [AdoMet] by a similar amount in histidine-fed cells there was little change in tumbling frequency. Intracellular [ATP] was reduced from 4.5 mM to less than 0.2 mM by histidine starvation. About 0.2 mM ATP was necessary for spontaneous tumbling. A similar [ATP] was required for tumbling in arsenate-treated cells. Adenine at concentrations as low as 20 nM caused a transient increase in both tumbling frequency and [ATP] in histidine-starved cells. Thus, out of three parameters tested, only the intracellular [ATP] correlated with changes in tumbling frequency in the histidine-starved cells.
有证据表明,除了趋化作用已知需要ATP来合成S-腺苷甲硫氨酸(AdoMet)和维持质子动力外,趋化作用还需要ATP或一种密切相关的代谢物。先前的研究表明,鼠伤寒沙门氏菌的hisF营养缺陷型在缺乏组氨酸时会出现翻滚和趋化作用丧失,以及ATP耗尽的情况(加洛韦,R. J.,和泰勒,B. L.(1980年)《细菌学杂志》144卷,1068 - 1075页)。在本研究中,对鼠伤寒沙门氏菌的hisF突变体的细胞内[AdoMet]、膜电位和[ATP]进行了测量。由[³H]四苯基鏻离子在细胞内外的分配所确定的膜电位,在pH 7.6时约为 - 150 mV,在组氨酸饥饿时并未降低,反而略有升高。饥饿期间,AdoMet的浓度从0.4 mM降至0.3 mM,但当使用AdoMet合成酶抑制剂环亮氨酸在组氨酸喂养的细胞中使[AdoMet]降低类似量时,翻滚频率几乎没有变化。组氨酸饥饿使细胞内[ATP]从4.5 mM降至低于0.2 mM。自发翻滚大约需要0.2 mM的ATP。砷酸盐处理的细胞翻滚也需要类似的[ATP]浓度。低至20 nM的腺嘌呤会使组氨酸饥饿细胞的翻滚频率和[ATP]短暂增加。因此,在测试的三个参数中,只有细胞内[ATP]与组氨酸饥饿细胞中翻滚频率的变化相关。