Yu Xiuping, Suzuki Kichiya, Wang Yongqing, Gupta Aparna, Jin Renjie, Orgebin-Crist Marie-Claire, Matusik Robert
Department of Urologic Surgery, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Mol Endocrinol. 2006 Oct;20(10):2418-31. doi: 10.1210/me.2006-0008. Epub 2006 Jun 1.
Murine epididymal retinoic acid-binding protein [or lipocalin 5 (Lcn5)] is synthesized and secreted by the principal cells of the mouse middle/distal caput epididymidis. A 5-kb promoter fragment of the Lcn5 gene can dictate androgen-dependent and epididymis region-specific gene expression in transgenic mice. Here, we reported that the 1.8-kb Lcn5 promoter confers epididymis region-specific gene expression in transgenic mice. To decipher the mechanism that directs transcription, 14 chimeric constructs that sequentially removed 100 bp of 1.8-kb Lcn5 promoter were generated and transfected into epididymal cells and nonepididymal cells. Transient transfection analysis revealed that 1.3 kb promoter fragment gave the strongest response to androgens. Between the 1.2-kb to 1.3-kb region, two androgen receptor (AR) binding sites were identified. Adjacent to AR binding sites, a Foxa2 [Fox (Forkhead box) subclass A] binding site was confirmed by gel shift assay. Similar Foxa binding sites were also found on the promoters of human and rat Lcn5, indicating the Foxa binding site is conserved among species. We previously reported that among the three members of Foxa family, Foxa1 and Foxa3 were absent in the epididymis whereas Foxa2 was detected in epididymal principal cells. Here, we report that Foxa2 displays a region-specific expression pattern along the epididymis: no staining observed in initial segment, light staining in proximal caput, gradiently heavier staining in middle and distal caput, and strongest staining in corpus and cauda, regions with little or no expression of Lcn5. In transient transfection experiments, Foxa2 expression inhibits AR induction of the Lcn5 promoter, which is consistent with the lack of expression of Lcn5 in the corpus and cauda. We conclude that Foxa2 functions as a repressor that restricts AR regulation of Lcn5 to a segment-specific pattern in the epididymis.
小鼠附睾视黄酸结合蛋白[或脂质运载蛋白5(Lcn5)]由小鼠附睾中/远侧头部的主细胞合成并分泌。Lcn5基因的一个5kb启动子片段可在转基因小鼠中决定雄激素依赖性和附睾区域特异性基因表达。在此,我们报道1.8kb的Lcn5启动子在转基因小鼠中赋予附睾区域特异性基因表达。为了解析指导转录的机制,构建了14个嵌合构建体,它们依次去除了1.8kb Lcn5启动子的100bp,并转染到附睾细胞和非附睾细胞中。瞬时转染分析显示,1.3kb启动子片段对雄激素的反应最强。在1.2kb至1.3kb区域之间,鉴定出两个雄激素受体(AR)结合位点。通过凝胶迁移试验证实,在AR结合位点附近有一个Foxa2[叉头框(Fox)A亚类]结合位点。在人和大鼠Lcn5的启动子上也发现了类似的Foxa结合位点,表明Foxa结合位点在物种间保守。我们之前报道,在Foxa家族的三个成员中,附睾中不存在Foxa1和Foxa3,而在附睾主细胞中检测到Foxa2。在此,我们报道Foxa2沿附睾呈现区域特异性表达模式:起始段未观察到染色,近侧头部浅染色,中侧和远侧头部染色逐渐加深,而在体部和尾部染色最强,这些区域Lcn5表达很少或不表达。在瞬时转染实验中,Foxa2表达抑制AR对Lcn5启动子的诱导,这与Lcn5在体部和尾部缺乏表达一致。我们得出结论,Foxa2作为一种阻遏物,将AR对Lcn5的调控限制在附睾的节段特异性模式。