Eisenbach M, Raz T, Ciobotariu A
Biochemistry. 1983 Jun 21;22(13):3293-8. doi: 10.1021/bi00282a039.
Attractants, in the presence of respiration and ATPase inhibitors, stimulate a hyperpolarization in Escherichia coli [Eisenbach, M. (1982) Biochemistry 21, 6818-6825]. In order to examine whether this hyperpolarization is correlated with chemotaxis, the effect of the attractant D-galactose and its analogues on the membrane potential of wild-type E. coli strains and some of their mutants was studied. The main observations were the following: (i) Wild-type cells became hyperpolarized by either galactose or its nonmetabolizable analogues, D-fucose and L-sorbose. (ii) A mutant defective in galactose metabolism became hyperpolarized by galactose. (iii) Inhibiting the galactose permease system did not prevent the hyperpolarization, rather it facilitated the observation of the hyperpolarization. (iv) Mutants unable to transport galactose via the methyl beta-galactoside (Mgl) transport system but having normal chemotaxis to galactose became normally hyperpolarized by D-fucose. (v) Mutants which cannot bind galactose were not hyperpolarized by galactose. (vi) The hyperpolarization in flaI mutants, in which the whole chemotaxis machinery is repressed, was reduced to 12-15% of the hyperpolarization in the parent strains. (vii) Nonattractant sugars did not stimulate hyperpolarization. It is concluded that the hyperpolarization is the consequence of neither galactose metabolism nor transport but rather is correlated with galactose taxis.
在存在呼吸和ATP酶抑制剂的情况下,引诱剂会刺激大肠杆菌产生超极化现象[艾森巴赫,M.(1982年)《生物化学》21卷,6818 - 6825页]。为了研究这种超极化是否与趋化性相关,研究了引诱剂D - 半乳糖及其类似物对野生型大肠杆菌菌株及其一些突变体膜电位的影响。主要观察结果如下:(i)野生型细胞会因半乳糖或其不可代谢的类似物D - 岩藻糖和L - 山梨糖而发生超极化。(ii)半乳糖代谢缺陷的突变体因半乳糖而发生超极化。(iii)抑制半乳糖通透酶系统并不能阻止超极化,反而有助于观察到超极化现象。(iv)无法通过甲基β - 半乳糖苷(Mgl)转运系统转运半乳糖但对半乳糖具有正常趋化性的突变体,会因D - 岩藻糖而正常地发生超极化。(v)无法结合半乳糖的突变体不会因半乳糖而发生超极化。(vi)在flaI突变体中,整个趋化机制受到抑制,其超极化程度降至亲本菌株超极化程度的12 - 15%。(vii)非引诱性糖类不会刺激超极化。结论是,超极化既不是半乳糖代谢的结果,也不是转运的结果,而是与半乳糖趋化性相关。