Hunter D R, Norberg C L, Segel I H
J Bacteriol. 1973 Jun;114(3):956-60. doi: 10.1128/jb.114.3.956-960.1973.
Cycloheximide (actidione) has an immediate inhibitory effect on amino acid transport by nitrogen-starved or carbon-starved mycelium suspended in phosphate buffer. High concentrations of phosphate alone are slightly inhibitory; cycloheximide appears to potentiate the effect of phosphate. Ca(2+) reverses the inhibition of transport caused by phosphate plus cycloheximide. Ca(2+) did not relieve the inhibition of protein synthesis. Cycloheximide promotes a continual uptake of (45)Ca(2+) by the mycelium. The cumulative results suggest that (i) membrane-bound Ca(2+) is involved in amino acid transport, (ii) cycloheximide labilizes the membrane-bound Ca(2+), and (iii) phosphate forms a complex with Ca(2+) making it unavailable for its role in transport. The effect of cycloheximide described above is observed within 1 to 2 min after addition of the antibiotic. This initial inhibition occurs more rapidly with 10(-3) M cycloheximide than with 10(-5) M cycloheximide. However, after a longer preincubation time, a curious inverse relationship between cycloheximide concentration and amino acid transport is observed. The mycelium incubated with 10(-5) M cycloheximide remains strongly inhibited (unless the antibiotic is washed away). The mycelium incubated with 10(-3) M cycloheximide recovers about 40% of the transport activity lost during the rapid initial phase. We have no obvious explanation for the inverse effect.
放线菌酮（放线菌抑制素）对悬浮于磷酸盐缓冲液中的氮饥饿或碳饥饿菌丝体的氨基酸转运有即时抑制作用。单独的高浓度磷酸盐有轻微抑制作用；放线菌酮似乎能增强磷酸盐的作用。Ca(2+)可逆转由磷酸盐加放线菌酮引起的转运抑制。Ca(2+)不能解除对蛋白质合成的抑制。放线菌酮促进菌丝体持续摄取(45)Ca(2+)。累积结果表明：(i)膜结合的Ca(2+)参与氨基酸转运；(ii)放线菌酮使膜结合的Ca(2+)不稳定；(iii)磷酸盐与Ca(2+)形成复合物，使其无法发挥转运作用。上述放线菌酮的作用在添加抗生素后1至2分钟内即可观察到。10(-3)M放线菌酮引起的初始抑制比10(-5)M放线菌酮更快。然而，预孵育时间更长后，观察到放线菌酮浓度与氨基酸转运之间存在奇特的反比关系。用10(-5)M放线菌酮孵育的菌丝体仍受到强烈抑制（除非洗去抗生素）。用10(-3)M放线菌酮孵育的菌丝体可恢复在快速初始阶段损失的约40%的转运活性。我们对这种反比效应没有明显的解释。
