Maenhaut-Michel G, Brandenburger A, Boiteux S
Mol Gen Genet. 1978 Jul 25;163(3):293-9. doi: 10.1007/BF00271958.
The inactivation of lambda repressor was followed by the specific DNA binding assay during the course of lysogenic induction provoked by incubation at 42 degrees C of an E. coli tif-1 lysogenic strain. The presence of up to 400 microgram/ml chloramphenicol during the inducing treatment did not impair the loss of repressor binding activity, whilst concentrations of 200 microgram/ml neomycin and 100 microgram/ml rifampicin effectively inhibited the inactivation of lambda repressor. Residual protein synthesis in the presence of chloramphenicol, neomycin and rifampicin was 5%, 5% and 27% respectively of that observed in the drug-free control. This residual synthesis did not appear to involve amplification of the X-protein. These results suggest that tif-mediated inactivation of the lambda repressor requires the activation of some specific gene(s), the translation of which appears to be resistant to chloramphenicol.
在42℃孵育大肠杆菌tif-1溶原性菌株引发溶原性诱导过程中,通过特异性DNA结合试验监测λ阻遏物的失活情况。诱导处理期间存在高达400微克/毫升的氯霉素不会损害阻遏物结合活性的丧失,而200微克/毫升新霉素和100微克/毫升利福平的浓度可有效抑制λ阻遏物的失活。在氯霉素、新霉素和利福平存在下的残余蛋白质合成分别为无药对照中观察到的5%、5%和27%。这种残余合成似乎不涉及X蛋白的扩增。这些结果表明,tif介导的λ阻遏物失活需要激活某些特定基因,这些基因的翻译似乎对氯霉素具有抗性。