Thompson S, Wiberg J S
J Virol. 1978 Feb;25(2):491-9. doi: 10.1128/JVI.25.2.491-499.1978.
Cold centrifugation of lysis-inhibited Escherichia coli B infected with wild-type T4D results in extensive lysis beginning around 20 min after infection at 37 degrees C. Infection with an e mutant, which fails to make lysozyme, prevents lysis, but does not prevent a marked loss of K+ and Mg3+. The t gene product, thought to disrupt the cytoplasmic membrane in natural lysis, is not required for this handling-induced cation loss or lysis. Three lines of evidence argue that late protein synthesis is required to develop this potential for cation loss; the potential does not develop in infections by: (i) mutants defective in DNA synthesis, (ii) mutants defective in gene 55, and (iii) wild-type T4 when chloramphenicol is added at 6 min after infection. All late mutants examined, which are blocked in the major pathways of morphogenesis, do not prevent development of the potential. The evidence argues for a new, late effect of T4 infection on the cytoplasmic membrane.
用野生型T4D感染受裂解抑制的大肠杆菌B后进行冷离心,在37℃感染约20分钟后开始出现广泛裂解。用e突变体感染,该突变体不能产生溶菌酶,可防止裂解,但不能防止K⁺和Mg³⁺的显著丢失。t基因产物被认为在自然裂解中破坏细胞质膜,但这种处理诱导的阳离子丢失或裂解不需要它。有三条证据表明需要晚期蛋白质合成来产生这种阳离子丢失的可能性;在以下感染中不会产生这种可能性:(i) DNA合成缺陷的突变体,(ii) 基因55缺陷的突变体,以及(iii) 感染后6分钟添加氯霉素时的野生型T4。所有检测的晚期突变体,它们在形态发生的主要途径中受阻,并不阻止这种可能性的发展。证据表明T4感染对细胞质膜有新的晚期效应。