Institut de Génétique Moléculaire de Montpellier, UMR5535, CNRS, 1919 route de Mende, 34293 Montpellier Cedex 5, France.
J Biol Chem. 2010 Feb 26;285(9):6552-62. doi: 10.1074/jbc.M109.032680. Epub 2010 Jan 6.
The c-Fos proto-oncogenic transcription factor defines a multigene family controlling many processes both at the cell and the whole organism level. To bind to its target AP-1/12-O-tetradecanoylphorbol-13-acetate-responsive element or cAMP-responsive element DNA sequences in gene promoters and exert its transcriptional part, c-Fos must heterodimerize with other bZip proteins, its best studied partners being the Jun proteins (c-Jun, JunB, and JunD). c-Fos expression is regulated at many transcriptional and post-transcriptional levels, yet little is known on how its localization is dynamically regulated in the cell. Here we have investigated its intranuclear mobility using fluorescence recovery after photobleaching, genetic, and biochemical approaches. Whereas monomeric c-Fos is highly mobile and distributed evenly with nucleolar exclusion in the nucleus, heterodimerization with c-Jun entails intranuclear redistribution and dramatic reduction in mobility of c-Fos caused by predominant association with the nuclear matrix independently of any binding to AP-1/12-O-tetradecanoylphorbol-13-acetate-responsive element or cAMP-responsive element sequences. In contrast to c-Jun, dimerization with JunB does not detectably affect c-Fos mobility. However, dimerization with JunB affects intranuclear distribution with significant differences in the localization of c-Fos.c-Jun and c-Fos.JunB dimers. Moreover, c-Jun and JunB exert comparable effects on another Fos family member, Fra-1. Thus, we report a novel regulation, i.e. differentially regulated intranuclear mobility and distribution of Fos proteins by their Jun partners, and suggest the existence of intranuclear storage sites for latent c-Fos.c-Jun AP-1 complexes. This may affect the numerous physiopathological functions these transcription factors control.
原癌基因 c-Fos 原代转录因子定义了一个多基因家族,该家族控制着细胞和整个生物体水平的许多过程。为了与基因启动子中的靶 AP-1/12-O-十四烷酰佛波醇-13-乙酸酯反应元件或 cAMP 反应元件 DNA 序列结合并发挥其转录功能,c-Fos 必须与其他 bZip 蛋白异二聚化,其研究最充分的伙伴是 Jun 蛋白(c-Jun、JunB 和 JunD)。c-Fos 的表达受到许多转录和转录后水平的调节,但对于其在细胞中的定位如何动态调节知之甚少。在这里,我们使用荧光恢复后光漂白、遗传和生化方法研究了其核内流动性。虽然单体 c-Fos 具有高度的流动性,并且均匀分布在核仁排除之外,但与 c-Jun 的异二聚化会导致核内重新分布,并由于与核基质的主要结合而导致 c-Fos 的流动性显著降低,而与 AP-1/12-O-十四烷酰佛波醇-13-乙酸酯反应元件或 cAMP 反应元件序列无关。与 c-Jun 不同,与 JunB 的二聚化不会明显影响 c-Fos 的流动性。然而,与 JunB 的二聚化会影响核内分布,导致 c-Fos 的定位有显著差异。c-Jun 和 c-Fos.JunB 二聚体。此外,c-Jun 和 JunB 对另一个 Fos 家族成员 Fra-1 产生类似的影响。因此,我们报告了一种新的调节机制,即 Fos 蛋白的 Jun 伴侣差异调节核内流动性和分布,并提出了潜在的 c-Fos.c-Jun AP-1 复合物的核内储存位点的存在。这可能会影响这些转录因子控制的许多生理病理功能。