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噬菌体T4衣壳长度决定的遗传学研究。II. 涉及特定蛋白质-蛋白质相互作用的遗传学证据。

Genetic studies on capsid-length determination in bacteriophage T4. II. Genetic evidence that specific protein-protein interactions are involved.

作者信息

Doherty D H

出版信息

J Virol. 1982 Aug;43(2):655-63. doi: 10.1128/JVI.43.2.655-663.1982.

Abstract

A bacteriophage T4 mutation (ptg19-80c) located in gene 23, which encodes the major structural protein of the T4 capsid, results in the production of capsids of abnormal length. Mutations outside gene 23 which partially suppress ptg19-80c have been described in the accompanying paper (D. H. Doherty, J. Virol. 43:641-654, 1982). Characterization of these suppressors was extended. A complementation test suggested that the suppressors were in genes 22 and 24. These genes coded for the major component of the morphogenetic core of the capsid precursor and the vertex protein of the capsid, respectively. The suppressor mutations were found to have no obvious phenotype in the absence of ptg19-80c. Suppression was shown to be allele specific: other ptg mutations at different sites in gene 23 were not suppressed by the suppressors of ptg19-80c. These results indicated that specific interactions among the three proteins gp22, gp23, and gp24 may play a role in the regulation of T4 capsid-length determination. Current models for capsid-length determination are considered in the light of these results.

摘要

位于基因23的噬菌体T4突变体(ptg19 - 80c)可编码T4衣壳的主要结构蛋白,该突变导致产生长度异常的衣壳。随附论文(D. H. Doherty,《病毒学杂志》43:641 - 654,1982年)中描述了基因23外部分抑制ptg19 - 80c的突变。对这些抑制子的特性描述进行了扩展。互补试验表明,这些抑制子存在于基因22和24中。这些基因分别编码衣壳前体形态发生核心的主要成分和衣壳顶点蛋白。发现抑制子突变在不存在ptg19 - 80c时没有明显表型。抑制作用显示为等位基因特异性:基因23中不同位点的其他ptg突变不会被ptg19 - 80c的抑制子所抑制。这些结果表明,三种蛋白gp22、gp23和gp24之间的特定相互作用可能在T4衣壳长度确定的调节中起作用。根据这些结果对当前衣壳长度确定模型进行了探讨。

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