Francis M K, Lehman J M
Department of Microbiology and Immunology, Albany Medical College, New York 12208.
Mol Cell Biol. 1989 Aug;9(8):3553-6. doi: 10.1128/mcb.9.8.3553-3556.1989.
Murine embryonal carcinoma F9 cells, a tissue culture model for early embryonic development, do not produce interferon (IFN) in response to poly(I-C), as determined by an antiviral assay. RNase protection analyses were used to examine total RNA extracted from the cells for the presence of beta-IFN RNA. Whereas F9 cells differentiated in vitro with retinoic acid produced a biologically active protein as well as beta-IFN RNA in response to poly(I-C), undifferentiated F9 cells produced no detectable beta-IFN RNA even in the presence of cycloheximide, an IFN-superinducing agent. These results show that undifferentiated embryonal carcinoma cells do not accumulate beta-IFN RNA in response to an IFN-inducing agent, suggesting a transcriptional regulatory mechanism. However, this control mechanism is altered upon differentiation, since the gene can be transcriptionally activated in retinoic acid-differentiated cells.
小鼠胚胎癌细胞F9是早期胚胎发育的组织培养模型,通过抗病毒试验测定,其对聚肌胞苷酸(poly(I-C))无反应,不产生干扰素(IFN)。采用核糖核酸酶保护分析来检测从细胞中提取的总RNA中是否存在β-干扰素RNA。用视黄酸在体外诱导分化的F9细胞,对聚肌胞苷酸有反应,能产生一种生物活性蛋白以及β-干扰素RNA,而未分化的F9细胞即使在存在干扰素超诱导剂环己酰亚胺的情况下,也检测不到β-干扰素RNA。这些结果表明,未分化的胚胎癌细胞对干扰素诱导剂无反应,不会积累β-干扰素RNA,提示存在转录调控机制。然而,这种调控机制在分化时会发生改变,因为该基因在视黄酸分化的细胞中可被转录激活。