Witmer H, Baros A, Forbes J, Padnos D, Maricondia W, Weiner M
J Gen Virol. 1976 Jun;31(3):289-302. doi: 10.1099/0022-1317-31-3-289.
Escherichia coli B/r (suo) was infected, at 30 degrees C, with T4Dam+, T4DamB24-amN82 (I-, 44-, DNA-negative phenotype), and T4DamN134amBL292 (33-, 55-, maturation-defective phenotype). A genetic ('transformation') assay was used to monitor transcription of genes 30 (polynucleotide ligase), 42 (deoxycytidylate hydroxymethylase), 43 (DNA polymerase), rIIA, rIIB, and e (endolysin). The principal results are: (I) All of the genes studied were transcribed exlusively from the so-called l-strand of phage DNA. (2) DNA synthesis and the maturation-defective proteins were required to turn-off transcription of genes 42, rIIA, tIIB, and 43. Experiments performed with chloramphenicol suggested that all phage-specific proteins required to turn-off transcription of these genes were not present until 6 to 8 min post infection (p.i.). (3) During a normal developmental programme, gene 30 was transcribed throughout the eclipse. DNA-negative and maturation-defective conditions had no obvious effect on transcription of this gene. (4) During a normal lytic event, two discrete waves of gene e transcription were observed. The late wave was dependent upon DNA-synthesis and presence of functional maturation-defective proteins. The early wave was unaffected by DNA-negative or maturation-defective conditions. Experiments with chloramphenicol indicated that, if any virus-specific proteins are involved with regulation of early e transcription, such proteins are present by 3 min p.i. The data are interpreted to mean that early gene transcription is regulated by a minimum of two mechanisms. One of these mechanisms is fully operational by the 3rd min and, among the genes studied, controlled early e transcription. A second mechanism becomes operational between 6 and 8 min p.i. and controls transcription of genes 42, 43, rIIA, and rIIB.
在30摄氏度下，用T4Dam +、T4DamB24 - amN82（I -，44 -，DNA阴性表型）和T4DamN134amBL292（33 -，55 -，成熟缺陷表型）感染大肠杆菌B/r（suo）。采用遗传（“转化”）测定法监测基因30（多核苷酸连接酶）、42（脱氧胞苷酸羟甲基化酶）、43（DNA聚合酶）、rIIA、rIIB和e（内溶素）的转录。主要结果如下：（1）所有研究的基因均仅从噬菌体DNA的所谓l链转录。（2）DNA合成和成熟缺陷蛋白是关闭基因42、rIIA、tIIB和43转录所必需的。用氯霉素进行的实验表明，直到感染后6至8分钟（p.i.）才出现关闭这些基因转录所需的所有噬菌体特异性蛋白。（3）在正常发育程序中，基因30在整个隐蔽期都进行转录。DNA阴性和成熟缺陷条件对该基因的转录没有明显影响。（4）在正常裂解过程中，观察到基因e转录有两个离散的波峰。晚期波峰依赖于DNA合成和功能性成熟缺陷蛋白的存在。早期波峰不受DNA阴性或成熟缺陷条件的影响。用氯霉素进行的实验表明，如果有任何病毒特异性蛋白参与早期e转录的调控，这些蛋白在感染后3分钟就已存在。这些数据被解释为意味着早期基因转录至少受两种机制调控。其中一种机制在第3分钟时完全起作用，在所研究的基因中，控制早期e转录。第二种机制在感染后6至8分钟之间起作用，并控制基因42、43、rIIA和rIIB的转录。
