Tabor H
Med Biol. 1981 Dec;59(5-6):389-93.
Previous work is summarized on the biosynthetic pathway for polyamines in Escherichia coli. Deletion mutants have been obtained in the various biosynthetic steps, resulting in cells with no polyamines. These mutants grow at one-third the rate of polyamine-supplemented cultures and can serve as suitable hosts for bacteriophages T4, T7, Q beta, and f2. The major effects of polyamine deficiency in these polyamine-deficient strains are: (i) these cells do not serve as hosts for bacteriophage gamma and (ii) polyamine-deficient male strains have defects which are attributable to a decrease in the stability of the male pili, namely, decreased numbers of recombinants in Hfr crosses and poorer adsorption of the male-specific bacteriophages f1, f2, and Q beta. One polyamine-deficient strain has been developed which becomes absolutely dependent on polyamines for growth if it also contains a specific rpsL (strA) mutation.
先前关于大肠杆菌中多胺生物合成途径的工作已被总结。在各个生物合成步骤中获得了缺失突变体,从而产生了不含多胺的细胞。这些突变体的生长速度是补充多胺培养物的三分之一,并且可以作为噬菌体T4、T7、Qβ和f2的合适宿主。这些多胺缺陷菌株中多胺缺乏的主要影响是:(i)这些细胞不能作为噬菌体γ的宿主;(ii)多胺缺陷的雄性菌株存在缺陷,这可归因于雄性菌毛稳定性的降低,即Hfr杂交中重组体数量减少以及雄性特异性噬菌体f1、f2和Qβ的吸附较差。已开发出一种多胺缺陷菌株,如果它还含有特定的rpsL(strA)突变,则其生长将绝对依赖于多胺。