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首页> 外文期刊>Journal of Cellular Physiology >A Functional N-terminal Domain in C/EBPβ-LAP* is Required for Interacting with SWI/SNF and to Repress Ric-8B Gene Transcription in Osteoblasts
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A Functional N-terminal Domain in C/EBPβ-LAP* is Required for Interacting with SWI/SNF and to Repress Ric-8B Gene Transcription in Osteoblasts

机译：函数n端结构域在C / EBPβ圈*与瑞士/ SNF和交互所必需的抑制Ric-8B成骨细胞的基因转录

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The chromatin remodeling complex SWI/SNF and the transcription factor C/EBPβ play critical roles in osteoblastic cells as they jointly control transcription of a number of bone-related target genes. The largest C/EBPβ isoform, LAP*, possesses a short additional N-terminal domain that has been proposed to mediate the interaction of this factor with SWI/SNF in myeloid cells. Here we examine the requirement of a functional N-terminus in C/EBPβ-LAP* for binding SWI/SNF and for recruiting this complex to the Ric-8B gene to mediate transcriptional repression. We find that both C/EBPβ-LAP* and SWI/SNF simultaneously bind to the Ric-8B promoter in differentiating osteoblasts that repress Ric-8B expression. This decreased expression of Ric-8B is not accompanied by significant changes in histone acetylation at the Ric-8B gene promoter sequence. A single aminoacid change at the C/EBPβ-LAP* N-terminus (R3L) that inhibits C/EBPβ-LAP*-SWI/SNF interaction, also prevents SWI/SNF recruitment to the Ric-8B promoter as well as C/EBPβ-LAP*-dependent repression of the Ric-8B gene. Inducible expression of the C/EBPβ-LAP*R3L protein in stably transfected osteoblastic cells demonstrates that this mutant protein binds to C/EBPβ-LAP*-target promoters and competes with the endogenous C/EBPβ factor. Together our results indicate that a functional N-terminus in C/EBPβ-LAP* is required for interacting with SWI/SNF and for Ric-8B gene repression in osteoblasts.
机译：染色质重塑复合物瑞士/ SNF和转录因子C / EBPβ扮演至关重要的角色在成骨细胞的细胞共同控制转录的骨的目标基因。拥有一个简短的额外的n端结构域提出了协调交互这个因素与瑞士/ SNF的骨髓细胞。我们检查功能的要求n端在C / EBPβ圈*瑞士/ SNF和绑定对招聘这一复杂Ric-8B基因调节转录镇压。两个C / EBPβ圈*和瑞士/ SNF同时绑定在区分Ric-8B启动子成骨细胞,抑制Ric-8B表达式。减少表达Ric-8B不是陪同组蛋白乙酰化作用的重大改变Ric-8B基因启动子序列。胺基酸变化在C / EBPβ圈* n端(R3L)抑制C / EBPβ圈*瑞士/ SNF相互作用,还可以防止瑞士/ SNF招聘Ric-8B发起人以及C / EBPβ圈*端依赖Ric-8B的镇压基因。蛋白质的稳定转染成骨细胞的细胞表明,这种突变蛋白结合C / EBPβ圈*—target推动者和竞争内生C / EBPβ因素。结果表明,n端功能C / EBPβ圈*需要互动瑞士/ SNF Ric-8B基因镇压造骨细胞。

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