Linder C H, Sköld O
J Virol. 1977 Jan;21(1):7-15. doi: 10.1128/JVI.21.1.7-15.1977.
Two forms of prereplicative phage RNA can be discerned in Escherichia coli early after infection with bacteriophage T4, immediate early and delayed early RNA. The transition from immediate early to delayed early RNA synthesis is inhibited by chloramphenicol. The present work presents evidence for the existence of a phage-specific protein, which effects this transition. Delayed early RNA formation was measured by a cistron-specific enzyme-forming-capacity method, in which RNA synthesized in the presence of chloramphenicol was allowed to express itself into enzyme activity after (i) the addition of rifampin to inhibit further transcription and (ii) subsequent removal of chloramphenicol. As representatives of delayed early transcription, the two phage-specific enzymes dCTPase and deoxynucleotide kinase were chosen. Primary infection with a phage mutant defective in one of these two enzymes was found to induce a diffusible factor, which in the presence of chloramphenicol could effect the formation of delayed early RNA corresponding to the missing enzyme, upon superinfection with wild-type phage. The activity of this factor, acting in trans, was abolished by the amino acid analogue ethionine. Mutation in the suA gene of the host did not relieve phage of the apparent need for protein synthesis in the transition from immediate early to delayed early phage RNA synthesis.
在大肠杆菌被噬菌体T4感染后的早期,可以识别出两种复制前噬菌体RNA形式,即立即早期RNA和延迟早期RNA。从立即早期RNA合成到延迟早期RNA合成的转变受到氯霉素的抑制。目前的工作提供了一种噬菌体特异性蛋白质存在的证据,该蛋白质影响这种转变。通过顺反子特异性酶形成能力方法测量延迟早期RNA的形成,其中在氯霉素存在下合成的RNA在(i)添加利福平以抑制进一步转录和(ii)随后去除氯霉素后被允许表达为酶活性。作为延迟早期转录的代表,选择了两种噬菌体特异性酶dCTPase和脱氧核苷酸激酶。发现用这两种酶之一有缺陷的噬菌体突变体进行初次感染会诱导一种可扩散因子,在氯霉素存在下,当用野生型噬菌体进行超感染时,该因子可影响对应于缺失酶的延迟早期RNA的形成。这种反式作用因子的活性被氨基酸类似物乙硫氨酸消除。宿主suA基因的突变并没有使噬菌体在从立即早期噬菌体RNA合成到延迟早期噬菌体RNA合成的转变中明显不再需要蛋白质合成。