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噬菌体λ的rex基因可在无噬菌体超感染的情况下抑制细胞功能。

The rex genes of bacteriophage lambda can inhibit cell function without phage superinfection.

作者信息

Snyder L, McWilliams K

机构信息

Department of Microbiology, Michigan State University, East Lansing 48824.

出版信息

Gene. 1989 Sep 1;81(1):17-24. doi: 10.1016/0378-1119(89)90332-6.

Abstract

The rexA and rexB genes of bacteriophage lambda are expressed from the prophage and cause the exclusion of many superinfecting mutant phages. We cloned the rexA and rexB genes into a multicopy plasmid so that they were overexpressed from the inducible tac promoter. No obvious phenotypes were associated with overexpressing both rexA and rexB or overexpressing rexA in the absence of rexB expression. However, induction of rexA in the presence of limiting rexB activity caused an immediate cessation of cell growth. All macromolecular synthesis abruptly ceased and amino acid transport was severely inhibited. Intracellular levels of adenosine 5'-triphosphate also dropped. These phenotypes are similar to those observed after phage superinfection, leading us to propose that at least some of the exclusion caused by the Rex proteins could be due to a change in their ratio following superinfection.

摘要

噬菌体λ的rexA和rexB基因由原噬菌体表达,并导致许多超感染突变噬菌体被排除。我们将rexA和rexB基因克隆到一个多拷贝质粒中,使其从可诱导的tac启动子过量表达。同时过量表达rexA和rexB或在不存在rexB表达的情况下过量表达rexA均未表现出明显的表型。然而,在rexB活性有限的情况下诱导rexA会导致细胞生长立即停止。所有大分子合成突然停止,氨基酸转运受到严重抑制。细胞内三磷酸腺苷水平也下降。这些表型与噬菌体超感染后观察到的表型相似,这使我们提出,Rex蛋白引起的至少部分排除可能是由于超感染后它们比例的变化。

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