Winter R B, Gold L
Cell. 1983 Jul;33(3):877-85. doi: 10.1016/0092-8674(83)90030-2.
Double-stranded cDNA from the maturation (or A2) protein gene of the RNA bacteriophage Q beta has been cloned such that its expression is regulated by the E. coli lac promoter/operator. Induction of the A2 clone is lethal to the host. The basis of this lethality is cell lysis, which is correlated with synthesis of the A2 protein. No other major proteins appear to be made from the A2 gene when inducer is added. Plasmid-derived A2 protein specifically complements infecting Q beta A2 amber mutants. Lysis activity is abolished in clones that synthesize truncated or internally deleted A2 polypeptides ranging from 10% to 95% of the length of wild-type protein. We conclude that host lysis is promoted by the maturation protein itself, rather than by a separate lysis protein. The A2 protein probably allows for the release of progeny Q beta phage particles following normal infection.
RNA噬菌体Qβ成熟(或A2)蛋白基因的双链cDNA已被克隆,其表达受大肠杆菌乳糖启动子/操纵子调控。A2克隆的诱导对宿主是致死的。这种致死性的基础是细胞裂解,这与A2蛋白的合成相关。添加诱导剂后,A2基因似乎不会产生其他主要蛋白质。质粒衍生的A2蛋白能特异性地互补感染性Qβ A2琥珀突变体。在合成截短或内部缺失的A2多肽(长度为野生型蛋白的10%至95%)的克隆中,裂解活性消失。我们得出结论,宿主裂解是由成熟蛋白本身促进的,而不是由单独的裂解蛋白促进的。A2蛋白可能在正常感染后允许子代Qβ噬菌体颗粒的释放。