Linder C H, Carlson K, Albertioni F, Söderström J, Påhlson C
Department of Pharmaceutical Biosciences, Faculty of Pharmacy, University of Uppsala, Sweden.
Genetics. 1994 Jul;137(3):613-25. doi: 10.1093/genetics/137.3.613.
A litCon mutation in Escherichia coli TU6 results in exclusion of bacteriophage T4 during the late, morphogenetic stage of its development at low temperatures. DNA was synthesized continuously in the infected cells, but less than 10% of the DNA made by 90 min after infection was packaged into DNAase-resistant particles, few viable phage were formed, and the cells lysed poorly. The exclusion could be relieved by conditions leading to elevated levels, determined immunologically, of the E. coli Rho protein (believed to be involved in regulation of T4 transcription), or chromosomally encoded E. coli GroEL (a chaperone known to be involved in phage assembly), or by supplying GroEL in trans from a plasmid. The two suppressing proteins appeared to act independently of each other. GroEL-suppression restored packaging to normal levels, perhaps by preventing GP23 from activating the host Lit protein; in addition DNA synthesis was delayed and reduced and cell lysis enhanced, demonstrating involvement of GroEL in both these processes. Rho suppression was less efficient. Since both transcription-termination-proficient and transcription-termination-deficient Rho suppressed, the results raise the possibility that Rho has a role during T4 development not directly involving transcription regulation.
大肠杆菌TU6中的litCon突变导致在低温下噬菌体T4发育的晚期形态发生阶段被排斥。感染细胞中DNA持续合成，但感染后90分钟内合成的DNA中不到10%被包装成抗DNA酶颗粒，形成的活噬菌体很少，细胞裂解也很差。通过导致大肠杆菌Rho蛋白（据信参与T4转录调控）或染色体编码的大肠杆菌GroEL（一种已知参与噬菌体组装的伴侣蛋白）水平升高的条件（通过免疫测定），或者通过从质粒反式提供GroEL，可以缓解这种排斥。这两种抑制蛋白似乎相互独立起作用。GroEL抑制可能通过阻止GP23激活宿主Lit蛋白将包装恢复到正常水平；此外，DNA合成延迟且减少，细胞裂解增强，表明GroEL参与了这两个过程。Rho抑制效率较低。由于转录终止能力强和转录终止缺陷的Rho都有抑制作用，结果增加了Rho在T4发育过程中具有不直接涉及转录调控作用的可能性。
