Analysis of the promoter from an expanding mouse retrotransposon subfamily
Analysis of the promoter from an expanding mouse retrotransposon subfamily
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DOI：
10.1006/geno.1998.5729
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发表时间：
1999-03-15
期刊：
影响因子：
4.4
通讯作者：
Kazazian, HH
中科院分区：
文献类型：
--
作者：
DeBerardinis, RJ;Kazazian, HH
小鼠基因组包含反转录转座子L1的几个亚家族。一个亚家族T-F包含4000-5000个全长成员，并且由于大量活性元件的反转录转座而正在扩展。在这里，我们研究了T-F 5'非翻译区（UTR），其中包含亚家族表达所需的启动子活性。使用报告基因分析，我们发现启动子活性来源于T-F特异性单体序列，并且与5' UTR中的单体数量成比例。这些数据表明，小鼠基因组中的几乎所有全长T-F元件目前都能够表达。我们比对了53个单体的序列以产生共有T-F单体，并确定大多数T-F元件在转录起始因子的潜在结合位点附近被截短。我们还确定T-F单体之间的大部分序列变异是由CpG二核苷酸的转换突变引起的，这表明基因组T-F 5'UTR在CpG处被甲基化。(C)北京：科学出版社.
The mouse genome contains several subfamilies of the retrotransposon L1. One subfamily, T-F, contains 4000-5000 full-length members and is expanding due to retrotransposition of a large number of active elements. Here we studied the T-F 5' untranslated region (UTR), which contains promoter activity required for subfamily expression. Using reporter assays, we show that promoter activity is derived from T-F-specific monomer sequences and is proportional to the number of monomers in the 5' UTR. These data suggest that nearly all full-length T-F elements in the mouse genome are currently competent for expression. We aligned the sequences of 53 monomers to generate a consensus T-F monomer and determined that most T-F elements are truncated near a potential binding site for a transcription initiation factor. We also determined that much of the sequence variation among T-F monomers results from transition mutations at CpG dinucleotides, suggesting that genomic T-F 5' UTRs are methylated at CpGs. (C) 1999 Academic Press.