Voss Ty C, Demarco Ignacio A, Booker Cynthia F, Day Richard N
Department of Medicine, University of Virginia, Charlottesville, VA 22908, USA.
J Cell Sci. 2005 Aug 1;118(Pt 15):3277-88. doi: 10.1242/jcs.02450. Epub 2005 Jul 19.
The co-repressor proteins SMRT and NCoR concentrate in specific subnuclear compartments and function with DNA-binding factors to inhibit transcription. To provide detailed mechanistic understanding of these activities, this study tested the hypothesis that functional interactions with transcription factors, such as the pituitary-gland-specific Pit-1 homeodomain protein, direct the subnuclear organization and activity of co-repressor complexes. Both SMRT and NCoR repressed Pit-1-dependent transcription, and NCoR was co-immunoprecipitated with Pit-1. Immunofluorescence experiments confirmed that endogenous NCoR is concentrated in small focal bodies and that incremental increases in fluorescent-protein-tagged NCoR expression lead to progressive increases in the size of these structures. In pituitary cells, the endogenous NCoR localized with endogenous Pit-1 and the co-expression of a fluorescent-protein-labeled Pit-1 redistributed both NCoR and SMRT into diffuse nucleoplasmic compartments that also contained histone deacetylase and chromatin. Automated image-analysis methods were applied to cell populations to characterize the reorganization of co-repressor proteins by Pit-1 and mutation analysis showed that Pit-1 DNA-binding activity was necessary for the reorganization of co-repressor proteins. These data support the hypothesis that spherical foci serve as co-repressor storage compartments, whereas Pit-1/co-repressor complexes interact with target genes in more widely dispersed subnuclear domains. The redistribution of co-repressor complexes by Pit-1 might represent an important mechanism by which transcription factors direct changes in cell-specific gene expression.
共抑制蛋白SMRT和NCoR集中在特定的核内亚区室,并与DNA结合因子共同发挥作用以抑制转录。为了详细了解这些活性的机制,本研究检验了以下假设:与转录因子(如垂体特异性Pit-1同源域蛋白)的功能相互作用指导了共抑制复合物的核内亚组织和活性。SMRT和NCoR均抑制Pit-1依赖性转录,且NCoR与Pit-1共免疫沉淀。免疫荧光实验证实,内源性NCoR集中在小的焦点体中,并且荧光蛋白标记的NCoR表达的逐步增加导致这些结构的大小逐渐增加。在垂体细胞中,内源性NCoR与内源性Pit-1共定位,荧光蛋白标记的Pit-1的共表达将NCoR和SMRT重新分布到也含有组蛋白脱乙酰酶和染色质的弥漫性核质区室中。将自动图像分析方法应用于细胞群体以表征Pit-1对共抑制蛋白的重组,突变分析表明Pit-1 DNA结合活性对于共抑制蛋白的重组是必需的。这些数据支持以下假设:球形焦点作为共抑制储存区室,而Pit-1/共抑制复合物在更广泛分散的核内亚域中与靶基因相互作用。Pit-1对共抑制复合物的重新分布可能代表转录因子指导细胞特异性基因表达变化的一种重要机制。