TIF-IA是介导核糖体RNA合成的生长依赖性调控的因子，是酵母Rrn3p的哺乳动物同源物。
TIF-IA, the factor mediating growth-dependent control of ribosomal RNA synthesis, is the mammalian homolog of yeast Rrn3p.
作者信息
Bodem J, Dobreva G, Hoffmann-Rohrer U, Iben S, Zentgraf H, Delius H, Vingron M, Grummt I
机构信息
Division of Molecular Biology of the Cell II, German Cancer Research Center, Heidelberg.
出版信息
EMBO Rep. 2000 Aug;1(2):171-5. doi: 10.1093/embo-reports/kvd032.
Abstract
Cells carefully modulate the rate of rRNA transcription in order to prevent an overinvestment in ribosome synthesis under less favorable nutritional conditions. In mammals, growth-dependent regulation of RNA polymerase I (Pol I) transcription is mediated by TIF-IA, an essential initiation factor that is active in extracts from growing but not starved or cycloheximide-treated mammalian cells. Here we report the molecular cloning and functional characterization of recombinant TIF-IA, which turns out to be the mammalian homolog of the yeast factor Rrn3p. We demonstrate that TIF-IA interacts with Pol I in the absence of template DNA, augments Pol I transcription in vivo and rescues transcription in extracts from growth-arrested cells in vitro.
摘要
细胞会仔细调节核糖体RNA（rRNA）的转录速率，以防止在营养条件较差的情况下对核糖体合成进行过度投入。在哺乳动物中，RNA聚合酶I（Pol I）转录的生长依赖性调节由TIF-IA介导，TIF-IA是一种必需的起始因子，在生长中的哺乳动物细胞提取物中具有活性，但在饥饿或经环己酰亚胺处理的细胞提取物中无活性。在此，我们报告了重组TIF-IA的分子克隆和功能特性，结果表明它是酵母因子Rrn3p的哺乳动物同源物。我们证明，TIF-IA在没有模板DNA的情况下与Pol I相互作用，在体内增强Pol I转录，并在体外拯救生长停滞细胞提取物中的转录。
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