Yazawa Takashi, Mizutani Tetsuya, Yamada Kazuya, Kawata Hiroko, Sekiguchi Toshio, Yoshino Miki, Kajitani Takashi, Shou Zhangfei, Miyamoto Kaoru
Department of Biochemistry, Fukui Medical University, Fukui 910-1193, Japan.
Endocrinology. 2003 May;144(5):1920-30. doi: 10.1210/en.2002-221070.
Upon FSH stimulation, many genes are acutely induced in granulosa cells. Gonadotropin-inducible ovarian transcription factor 1 (GIOT1) represents a novel member of the group of transcriptional repressors that belong to one such gene. To investigate the mechanism of this transcriptional activation, a rat GIOT1 promoter region was isolated and subsequently ligated to a luciferase vector and transfected to freshly prepared granulosa cells. A luciferase reporter gene driven by 0.8 kb of the GIOT1 5'-flanking region was highly expressed in response to FSH. Deletion and mutational analyses indicated that two response elements, including a steroidogenic factor 1 (SF-1) site and a cAMP response element (CRE), are required for the activation of the gene by FSH. Gel shift experiments also indicated that SF-1 and CRE binding protein specifically bind to each site. To reveal the relationship between SF-1 and the cAMP-dependent protein kinase A pathway, cotransfection was performed using SF-1-deficient cells. Although SF-1 and the catalytic subunit of protein kinase A individually caused a modest stimulation of the GIOT1 promoter, dramatic synergistic effects were observed in the case of cotransfection. Although the amount of SF-1 remained unchanged in response to FSH in granulosa cells, Dax-1 expression immediately decreased. The ectopic expression of Dax-1 inhibited the SF-1-dependent GIOT1 promoter activity. These results suggest that the synergistic action of CRE binding protein and SF-1 and the rapid down-regulation of Dax-1 are responsible for the acute induction of GIOT1 gene by gonadotropin.
在促卵泡激素(FSH)刺激下,颗粒细胞中许多基因会被迅速诱导表达。促性腺激素诱导的卵巢转录因子1(GIOT1)是属于此类基因的转录抑制因子组中的一个新成员。为了研究这种转录激活的机制,分离了大鼠GIOT1启动子区域,随后将其连接到荧光素酶载体上,并转染到新制备的颗粒细胞中。由GIOT1 5'侧翼区域的0.8 kb驱动的荧光素酶报告基因在FSH刺激下高度表达。缺失和突变分析表明,FSH激活该基因需要两个反应元件,包括一个类固醇生成因子1(SF-1)位点和一个cAMP反应元件(CRE)。凝胶迁移实验也表明,SF-1和CRE结合蛋白特异性结合到每个位点。为了揭示SF-1与cAMP依赖性蛋白激酶A途径之间的关系,使用缺乏SF-1的细胞进行了共转染实验。尽管SF-1和蛋白激酶A的催化亚基单独对GIOT1启动子有适度的刺激作用,但在共转染时观察到了显著的协同效应。尽管颗粒细胞中SF-1的量在FSH刺激下保持不变,但Dax-1的表达立即下降。Dax-1的异位表达抑制了SF-1依赖性GIOT1启动子活性。这些结果表明,CRE结合蛋白和SF-1的协同作用以及Dax-1的快速下调是促性腺激素对GIOT1基因急性诱导的原因。