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衣壳蛋白的合成抑制了噬菌体T3突变体的发育,这些突变体会流产感染含有F质粒的细胞。

Synthesis of the capsid protein inhibits development of bacteriophage T3 mutants that abortively infect F plasmid-containing cells.

作者信息

Condreay J P, Molineux I J

机构信息

Department of Microbiology, University of Texas, Austin 78712.

出版信息

J Mol Biol. 1989 Jun 5;207(3):543-54. doi: 10.1016/0022-2836(89)90463-4.

Abstract

Mutants of bacteriophage T3 that lack gene 1.2 resemble wild-type phage T7 in that they are unable productively to infect F plasmid-containing cells of Escherichia coli. Pseudorevertants of a T3 gene 1.2 deletion mutant that have regained the ability to plate efficiently on male cells have been isolated and characterized. At least two mutations in the gene for the major capsid protein are necessary for these phages to bypass F-mediated restriction. One mutation serves to reduce the rate of synthesis of the capsid protein; a second mutation apparently alters an unknown property that is intrinsic to the free, or unassembled form of the protein. During the abortive infection of an F-containing host, synthesis of the wild-type capsid protein directly inhibits further phage development.

摘要

缺乏基因1.2的噬菌体T3突变体与野生型噬菌体T7相似,因为它们无法有效地感染含有F质粒的大肠杆菌细胞。已分离并鉴定出T3基因1.2缺失突变体的假回复体,这些假回复体重新获得了在雄性细胞上高效平板形成的能力。这些噬菌体绕过F介导的限制需要主要衣壳蛋白基因中的至少两个突变。一个突变用于降低衣壳蛋白的合成速率;第二个突变显然改变了蛋白质游离或未组装形式所固有的未知特性。在含F宿主的流产感染过程中,野生型衣壳蛋白的合成直接抑制了噬菌体的进一步发育。

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