Kang S, Markovitz A
J Bacteriol. 1967 Feb;93(2):584-91. doi: 10.1128/jb.93.2.584-591.1967.
Escherichia coli K-12 strain AB259 can be induced to form capsular polysaccharide (mucoid clones) by dl-p-fluorophenylalanine (FPA; 5 x 10(-6)m on agar plates at 37 C or 8 x 10(-5)m in liquid medium at 30 C). The change was shown to be phenotypic. An increase in enzymes probably involved in capsular polysaccharide synthesis [phosphomannose isomerase (3.3-fold), uridine diphosphate-d-galactose-4-epimerase (2.5-fold), and guanine diphosphate-l-fucose synthetase] was demonstrated as a result of growth in FPA. These increases appear sufficient to account for the increased synthesis of capsular polysaccharide due to growth in FPA. FPA-resistant derivatives of strain AB259 were obtained by selecting mutants on FPA-containing agar or by transducing in an altered phenylalanyl soluble ribonucleic acid synthetase that activates FPA poorly. Mucoid clones were formed by these strains only in the presence of 30 to 1,000 times as much FPA. Among these strains, there was a close correlation between incorporation of FPA-C(14) and induction of capsular polysaccharide synthesis. The results are thus consistent with the following model: FPA is incorporated into the protein product of the R(1) gene (repressor) and alters it sufficiently to allow derepression of several enzymes.
大肠杆菌K-12菌株AB259可通过dl-对氟苯丙氨酸(FPA;在37℃的琼脂平板上为5×10⁻⁶m,在30℃的液体培养基中为8×10⁻⁵m)诱导形成荚膜多糖(黏液样克隆)。这种变化被证明是表型的。由于在FPA中生长,参与荚膜多糖合成的酶[磷酸甘露糖异构酶(3.3倍)、尿苷二磷酸-d-半乳糖-4-表异构酶(2.5倍)和鸟苷二磷酸-L-岩藻糖合成酶]增加。这些增加似乎足以解释由于在FPA中生长导致的荚膜多糖合成增加。通过在含FPA的琼脂上选择突变体或转导一种激活FPA能力差的改变的苯丙氨酰可溶性核糖核酸合成酶,获得了菌株AB259的FPA抗性衍生物。这些菌株仅在存在30至1000倍量FPA的情况下形成黏液样克隆。在这些菌株中,FPA-C¹⁴的掺入与荚膜多糖合成的诱导之间存在密切相关性。因此,结果与以下模型一致:FPA被掺入R₁基因(阻遏物)的蛋白质产物中,并对其进行充分改变以允许几种酶的去阻遏。