Myers C A, Schmidhauser C, Mellentin-Michelotti J, Fragoso G, Roskelley C D, Casperson G, Mossi R, Pujuguet P, Hager G, Bissell M J
Life Sciences Division, Berkeley National Laboratory, California 94720, USA.
Mol Cell Biol. 1998 Apr;18(4):2184-95. doi: 10.1128/MCB.18.4.2184.
We have previously described a 160-bp enhancer (BCE-1) in the bovine beta-casein gene that is activated in the presence of prolactin and extracellular matrix (ECM). Here we report the characterization of the enhancer by deletion and site-directed mutagenesis, electrophoretic mobility shift analysis, and in vivo footprinting. Two essential regions were identified by analysis of mutant constructions: one binds C/EBP-beta and the other binds MGF/STAT5 and an as-yet-unidentified binding protein. However, no qualitative or quantitative differences in the binding of these proteins were observed in electrophoretic mobility shift analysis using nuclear extracts derived from cells cultured in the presence or absence of ECM with or without prolactin, indicating that prolactin- and ECM-induced transcription was not dependent on the availability of these factors in the functional cell lines employed. An in vivo footprinting analysis of the factors bound to nuclear chromatin in the presence or absence of ECM and/or prolactin found no differences in the binding of C/EBP-beta but did not provide definitive results for the other factors. Neither ECM nor prolactin activated BCE-1 in transient transfections, suggesting that the chromosomal structure of the integrated template may be required for ECM-induced transcription. Further evidence is that treatment of cells with inhibitors of histone deacetylase was sufficient to induce transcription of integrated BCE-1 in the absence of ECM. Together, these results suggest that the ECM induces a complex interaction between the enhancer-bound transcription factors, the basal transcriptional machinery, and a chromosomally integrated template responsive to the acetylation state of the histones.
我们之前曾描述过牛β-酪蛋白基因中的一个160bp增强子(BCE-1),它在催乳素和细胞外基质(ECM)存在的情况下被激活。在此,我们报告通过缺失和定点诱变、电泳迁移率变动分析及体内足迹法对该增强子的特性研究。通过对突变构建体的分析鉴定出两个关键区域:一个区域结合C/EBP-β,另一个区域结合MGF/STAT5以及一种尚未鉴定的结合蛋白。然而,在使用来自有无ECM和有无催乳素培养的细胞的核提取物进行的电泳迁移率变动分析中,未观察到这些蛋白结合存在定性或定量差异,这表明催乳素和ECM诱导的转录不依赖于所用功能细胞系中这些因子的可利用性。对有无ECM和/或催乳素时与核染色质结合的因子进行的体内足迹分析发现,C/EBP-β的结合没有差异,但对其他因子未得出明确结果。在瞬时转染中,ECM和催乳素均未激活BCE-1,这表明ECM诱导的转录可能需要整合模板的染色体结构。进一步的证据是,在无ECM的情况下,用组蛋白脱乙酰酶抑制剂处理细胞足以诱导整合的BCE-1转录。总之,这些结果表明,ECM诱导增强子结合的转录因子、基础转录机制以及对组蛋白乙酰化状态有反应的染色体整合模板之间发生复杂相互作用。