Holt J T
Department of Cell Biology, Vanderbilt University, Medical School, Nashville, Tennessee 37232.
Mol Cell Biol. 1993 Jun;13(6):3821-30. doi: 10.1128/mcb.13.6.3821-3830.1993.
Serum induces the expression of a number of proteins with similar transcriptional properties, including those encoded by the proto-oncogenes c-fos and c-jun. This study employs a novel antisense rescue method to determine whether antisense-resistant genes (constructed by deletion of antisense RNA target sequences) can replace c-fos expression during serum-induced DNA synthesis. Immunoprecipitation studies and nuclease protection assays demonstrated that anti-fos RNA inhibited endogenous c-fos expression but did not inhibit expression of transfected antisense-resistant mutant c-fos genes. The results of nuclear-labelling and cellular-proliferation studies indicated that C terminally truncated Fos mutants, including FBR v-fos, could not rescue endogenous Fos, although full-length and minimally truncated c-fos expression vectors could restore serum-induced DNA synthesis in cells expressing anti-fos RNA. Overexpression of c-Jun protein (Jun) could not restore serum-induced DNA synthesis to cells expressing inducible anti-fos RNA despite equivalent transactivation of an AP-1 target gene. Thus, the antisense rescue method defines a specialized function for c-Fos protein which is distinct from the function(s) of Jun and/or transforming FBR v-Fos proteins.
血清可诱导多种具有相似转录特性的蛋白质表达,包括原癌基因c-fos和c-jun所编码的蛋白质。本研究采用一种新型的反义拯救方法,以确定抗反义基因(通过缺失反义RNA靶序列构建)在血清诱导的DNA合成过程中是否能够替代c-fos的表达。免疫沉淀研究和核酸酶保护试验表明,抗fos RNA抑制内源性c-fos表达,但不抑制转染的抗反义突变c-fos基因的表达。核标记和细胞增殖研究结果表明,C末端截短的Fos突变体,包括FBR v-fos,不能拯救内源性Fos,尽管全长和最小截短的c-fos表达载体能够在表达抗fos RNA的细胞中恢复血清诱导的DNA合成。尽管AP-1靶基因的反式激活作用相当,但c-Jun蛋白(Jun)的过表达不能恢复血清诱导的DNA合成至表达诱导型抗fos RNA的细胞中。因此,反义拯救方法确定了c-Fos蛋白的一种特殊功能,该功能不同于Jun和/或转化型FBR v-Fos蛋白的功能。