Ezashi T, Ghosh D, Roberts R M
Department of Animal Sciences and Biochemistry, University of Missouri, Columbia, Missouri 65211, USA.
Mol Cell Biol. 2001 Dec;21(23):7883-91. doi: 10.1128/MCB.21.23.7883-7891.2001.
Oct-4 is a POU family transcription factor associated with potentially totipotent cells. Genes expressed in the trophectoderm but not in embryos prior to blastocyst formation may be targets for silencing by Oct-4. Here, we have tested this hypothesis with the tau interferon genes (IFNT genes), which are expressed exclusively in the trophectoderm of bovine embryos. IFNT promoters contain an Ets-2 enhancer, located at -79 to -70, and are up-regulated about 20-fold by the overexpression of Ets-2 in human JAr choriocarcinoma cells, which are permissive for IFNT expression. This enhancement was reversed in a dose-dependent manner by coexpression of Oct-4 but not either Oct-1 or Oct-2. When cells were transfected with truncated bovine IFNT promoters designed to eliminate potential octamer sites sequentially, luciferase reporter expression from each construct was still silenced by Oct-4. Full repression required both the N-terminal and POU domains of Oct-4, but neither domain used alone was an effective silencer. Oct-4 and Ets-2 formed a complex in vitro in the absence of DNA through binding of the POU domain of Oct-4 to a site located between the "pointed" and DNA binding domains of Ets-2. The two transcription factors were also coimmunoprecipitated after being expressed together in JAr cells. Oct-4, therefore, silences IFNT promoters by quenching Ets-2 transactivation. The POU domain most probably binds to Ets-2 directly, while the N-terminal domain inhibits transcription. These findings provide further evidence that the developmental switch to the trophectoderm is accompanied by the loss of Oct-4 silencing of key genes.
Oct-4是一种与潜在全能细胞相关的POU家族转录因子。在囊胚形成之前,滋养外胚层中表达但胚胎中不表达的基因可能是Oct-4沉默的靶标。在这里,我们用tau干扰素基因(IFNT基因)验证了这一假设,该基因仅在牛胚胎的滋养外胚层中表达。IFNT启动子包含一个位于-79至-70的Ets-2增强子,在允许IFNT表达的人JAr绒毛膜癌细胞中,Ets-2的过表达可使其上调约20倍。Oct-4的共表达以剂量依赖的方式逆转了这种增强作用,而Oct-1或Oct-2则没有这种作用。当用设计用于依次消除潜在八聚体位点的截短牛IFNT启动子转染细胞时,每个构建体的荧光素酶报告基因表达仍被Oct-4沉默。完全抑制需要Oct-4的N末端和POU结构域,但单独使用任何一个结构域都不是有效的沉默子。在没有DNA的情况下,Oct-4和Ets-2在体外通过Oct-4的POU结构域与Ets-2的“尖”结构域和DNA结合结构域之间的位点结合形成复合物。在JAr细胞中共同表达后,这两种转录因子也被共免疫沉淀。因此,Oct-4通过淬灭Ets-2反式激活来沉默IFNT启动子。POU结构域很可能直接与Ets-2结合,而N末端结构域抑制转录。这些发现进一步证明,向滋养外胚层的发育转变伴随着关键基因Oct-4沉默的丧失。