Rutberg B, Rutberg L
J Bacteriol. 1966 Jan;91(1):76-80. doi: 10.1128/jb.91.1.76-80.1966.
Rutberg, Blanka (Karolinska Institutet, Stockholm, Sweden), and Lars Rutberg. Bacteriophage-induced functions in Escherichia coli K(lambda) infected with rII mutants of bacteriophage T4. J. Bacteriol. 91:76-80. 1966.-When Escherichia coli K(lambda) was infected with rII mutants of phage T4, deoxycytidine triphosphatase, one of the phage-induced early enzymes, was produced at initially the same rate as in r(+)-infected cells. Deoxyribonuclease activity was one-third to one-half of that of r(+)-infected cells. This lower deoxyribonuclease activity was observed also in other hosts or when infection was made with rI or rIII mutants. Presence of chloramphenicol did not allow a continued synthesis of phage deoxyribonucleic acid in rII-infected K(lambda). No phage lysozyme was detected nor was any antiphage serum-blocking antigen found in rII-infected K(lambda). It is suggested that the rII gene is of significance for the expression of phage-induced late functions in the host K(lambda).
鲁特伯格，布兰卡（瑞典斯德哥尔摩卡罗林斯卡学院）和拉尔斯·鲁特伯格。噬菌体T4的rII突变体感染大肠杆菌K（λ）后诱导产生的功能。《细菌学杂志》91:76 - 80。1966年。——当用噬菌体T4的rII突变体感染大肠杆菌K（λ）时，脱氧胞苷三磷酸酶作为噬菌体诱导产生的早期酶之一，最初的产生速率与感染r（+）的细胞相同。脱氧核糖核酸酶活性为感染r（+）细胞的三分之一到二分之一。在其他宿主中，或者用rI或rIII突变体进行感染时，也观察到这种较低的脱氧核糖核酸酶活性。氯霉素的存在不允许在rII感染的K（λ）中持续合成噬菌体脱氧核糖核酸。在rII感染的K（λ）中未检测到噬菌体溶菌酶，也未发现任何抗噬菌体血清阻断抗原。有人提出，rII基因对于宿主K（λ）中噬菌体诱导产生的晚期功能的表达具有重要意义。
