Yeilding N M, Lee W M
Department of Medicine and Cancer Center, University of Pennsylvania, Philadelphia 19104, USA.
Mol Cell Biol. 1997 May;17(5):2698-707. doi: 10.1128/MCB.17.5.2698.
Downregulation in expression of the c-myc proto-oncogene is an early molecular event in differentiation of murine C2C12 myoblasts into multinucleated myotubes. During differentiation, levels of c-myc mRNA decrease 3- to 10-fold despite a lack of change in its transcription rate. To identify cis-acting elements that target c-myc mRNA for downregulation during myogenesis, we stably transfected C2C12 cells with mutant myc genes or chimeric genes in which various myc sequences were fused to the human beta-globin gene or to the bacterial chloramphenicol acetyltransferase (CAT) gene. Deletion of coding sequences from myc exon 2 or exon 3 abolished downregulation of myc mRNA during myogenic differentiation, while deletion of introns or sequences in the 5' or 3' untranslated regions (UTRs) did not, demonstrating that coding elements in both exons 2 and 3 are necessary for myc mRNA downregulation. Fusion of coding sequences from either myc exon 2 or 3 to beta-globin mRNA conferred downregulation onto the chimeric mRNA, while fusion of myc 3' UTR sequences or coding sequences from CAT or ribosomal protein L32 did not, demonstrating that coding elements in myc exons 2 and 3 specifically confer downregulation. These results present the apparent paradox that coding elements in either myc exon 2 or myc exon 3 are sufficient to confer downregulation onto beta-globin mRNA, but neither element alone was sufficient for myc mRNA downregulation, suggesting that some feature of beta-globin mRNA may potentiate the regulatory properties of myc exons 2 and 3. A similar regulatory function is not shared by all mRNAs because fusion of either myc exon 2 or myc exon 3 to CAT mRNA did not confer downregulation onto the chimeric mRNA, but fusion of the two elements together did. We conclude from these results that two myc regulatory elements, one exon 2 and one in exon 3, are required for myc mRNA downregulation. Finally, using a highly sensitive and specific PCR-based assay for comparing mRNA levels, we demonstrated that the downregulation mediated by myc exons 2 and 3 results in a decrease in cytoplasmic mRNA levels, but not nuclear mRNA levels, indicating that regulation is a postnuclear event.
原癌基因c-myc表达的下调是小鼠C2C12成肌细胞分化为多核肌管过程中的早期分子事件。在分化过程中,尽管c-myc mRNA的转录速率没有变化,但其水平却下降了3至10倍。为了鉴定在肌生成过程中靶向c-myc mRNA进行下调的顺式作用元件,我们用突变的myc基因或嵌合基因稳定转染C2C12细胞,其中各种myc序列与人类β-珠蛋白基因或细菌氯霉素乙酰转移酶(CAT)基因融合。从myc外显子2或外显子3中删除编码序列消除了肌生成分化过程中myc mRNA的下调,而删除内含子或5'或3'非翻译区(UTR)中的序列则没有,这表明外显子2和3中的编码元件对于myc mRNA的下调是必需的。将myc外显子2或3的编码序列与β-珠蛋白mRNA融合可使嵌合mRNA下调,而将myc 3'UTR序列或CAT或核糖体蛋白L32的编码序列融合则不能,这表明myc外显子2和3中的编码元件特异性地导致下调。这些结果呈现出一个明显的悖论,即myc外显子2或myc外显子3中的编码元件足以使β-珠蛋白mRNA下调,但单独任何一个元件都不足以使myc mRNA下调,这表明β-珠蛋白mRNA的某些特征可能增强了myc外显子2和3的调节特性。并非所有mRNA都具有类似的调节功能,因为将myc外显子2或myc外显子3与CAT mRNA融合都不会使嵌合mRNA下调,但将这两个元件一起融合则会。我们从这些结果得出结论,myc mRNA下调需要两个myc调节元件,一个在外显子2中,一个在外显子3中。最后,使用一种高度灵敏且特异的基于PCR的方法来比较mRNA水平,我们证明由myc外显子2和3介导的下调导致细胞质mRNA水平降低,但不影响核mRNA水平,这表明调节是核后事件。