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脑膜炎奈瑟菌中Opc外膜蛋白的可变表达是由含有聚胞苷的启动子大小变异引起的。

Variable expression of the Opc outer membrane protein in Neisseria meningitidis is caused by size variation of a promoter containing poly-cytidine.

作者信息

Sarkari J, Pandit N, Moxon E R, Achtman M

机构信息

Max-Planck Institut für molekulare Genetik, Berlin, Germany.

出版信息

Mol Microbiol. 1994 Jul;13(2):207-17. doi: 10.1111/j.1365-2958.1994.tb00416.x.

Abstract

Opa proteins of Neisseria meningitidis exhibit translational phase variation via addition or deletion of repetitive coding repeat units within the DNA encoding the protein leader sequence. In contrast, Opc phase variation is the result of transcriptional regulation. Transcription starts 13 nucleotides after the -10 region of an unusual promoter sequence containing a variable number of contiguous cytidine residues and lacking a -35 region. Efficient expression of Opc occurred in strains with 12 to 13 cytidine residues, intermediate expression in strains with 11 or 14 residues and no expression with < or = 10 or > or = 15 residues. This unusual regulation may have evolved because the Opc protein enables meningococcal invasion and is immunogenic.

摘要

脑膜炎奈瑟菌的Opa蛋白通过在编码蛋白前导序列的DNA内重复编码重复单元的添加或缺失表现出翻译相位变异。相比之下,Opc相位变异是转录调控的结果。转录起始于一个不寻常启动子序列的-10区域后13个核苷酸处,该启动子序列含有可变数量的连续胞嘧啶残基且缺乏-35区域。Opc在含有12至13个胞嘧啶残基的菌株中高效表达,在含有11或14个残基的菌株中中等表达,在≤10或≥15个残基时无表达。这种不寻常的调控可能是因为Opc蛋白能使脑膜炎奈瑟菌侵入且具有免疫原性而进化而来。

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