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增强或抑制SV40主要晚期RNA转录的位点特异性碱基置换和缺失突变。

Site-specific base substitution and deletion mutations that enhance or suppress transcription of the SV40 major late RNA.

作者信息

Brady J, Radonovich M, Vodkin M, Natarajan V, Thoren M, Das G, Janik J, Salzman N P

出版信息

Cell. 1982 Dec;31(3 Pt 2):625-33. doi: 10.1016/0092-8674(82)90318-x.

DOI:10.1016/0092-8674(82)90318-x
PMID:7159930
Abstract

Transcriptional analysis of SV40 late promoter mutants indicates that the DNA sequence 5'-GGTACCTAACC-3' (map positions 294-304) is important in the control of SV40 late RNA expression. C to T base substitutions at map positions 298, 299 and 304 increased initiation of late RNA synthesis at map position 325 five to ten fold. G to A base substitutions at map positions 294 and 295 decreased RNA initiation by a factor of 2 to 3. Deletion of nucleotides 295-298 reduced RNA initiation by a factor of 4 to 5. S1 analysis of in vivo RNA, isolated 24-36 hr after infection, demonstrated that the four base deletion not only decreased RNA initiation at nucleotide 325, but also increased RNA initiation at three alternate sites located approximately 125 nucleotides upstream from the major late RNA initiation site.

摘要

SV40晚期启动子突变体的转录分析表明,DNA序列5'-GGTACCTAACC-3'(图谱位置294 - 304)在SV40晚期RNA表达的调控中起重要作用。图谱位置298、299和304处的C到T碱基替换使图谱位置325处晚期RNA合成的起始增加了5到10倍。图谱位置294和295处的G到A碱基替换使RNA起始减少了2到3倍。核苷酸295 - 298缺失使RNA起始减少了4到5倍。对感染后24 - 36小时分离的体内RNA进行S1分析表明,四个碱基的缺失不仅降低了核苷酸325处的RNA起始,还增加了位于主要晚期RNA起始位点上游约125个核苷酸处的三个替代位点的RNA起始。

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