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体内大肠菌素E3诱导的16S核糖体RNA的特异性失活

Specific inactivation of 16S ribosomal RNA induced by colicin E3 in vivo.

作者信息

Bowman C M, Dahlberg J E, Ikemura T, Konisky J, Nomura M

出版信息

Proc Natl Acad Sci U S A. 1971 May;68(5):964-8. doi: 10.1073/pnas.68.5.964.

Abstract

Treatment of sensitive Escherichia coli cells with colicin E3 leads to inactivation of 30S ribosomal subunits. In vitro reconstitution of 30S subunits indicates that the E3-induced defect lies solely in the 16S RNA. 16S RNA from E3-treated cells lacks several T(1) RNase oligonucleotides of normal 16S RNA, including the one from the 3'-end of the 16S RNA, as analyzed by the fingerprint technique of Sanger. An RNA fragment about 50 nucleotides long has been isolated from E3-treated cells. This RNA contains the original 3'-terminal oligonucleotide and other oligonucleotides missing in the E3-16S RNA. The results show that colicin E3 treatment causes the cleavage of 16S RNA at a specific position near the 3'-terminus.

摘要

用大肠杆菌素E3处理敏感的大肠杆菌细胞会导致30S核糖体亚基失活。30S亚基的体外重建表明,E3诱导的缺陷仅存在于16S RNA中。通过桑格指纹技术分析,来自E3处理细胞的16S RNA缺少正常16S RNA的几个T(1)核糖核酸酶寡核苷酸,包括来自16S RNA 3'端的那个。从E3处理的细胞中分离出了一个约50个核苷酸长的RNA片段。该RNA包含原始的3'末端寡核苷酸和E3-16S RNA中缺失的其他寡核苷酸。结果表明,大肠杆菌素E3处理导致16S RNA在靠近3'末端的特定位置发生切割。

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