Equipe labellisée par la Ligue Nationale contre le Cancer, Institut de Génétique Moléculaire de Montpellier UMR 5535 CNRS, 1919 route de Mende, 34293 Montpellier cedex 5, France, Université Montpellier 2, Place Eugène Bataillon, 34095 Montpellier cedex 5, France and Université Montpellier 1, 5 Bd Henry IV, 34967 Montpellier cedex 2, France.
Nucleic Acids Res. 2013 Oct;41(19):8908-25. doi: 10.1093/nar/gkt669. Epub 2013 Aug 5.
The junb gene behaves as an immediate early gene in bacterial lipopolysaccharide (LPS)-stimulated dendritic cells (DCs), where its transient transcriptional activation is necessary for the induction of inflammatory cytokines. junb is a short gene and its transcriptional activation by LPS depends on the binding of NF-κB to an enhancer located just downstream of its 3' UTR. Here, we have addressed the mechanisms underlying the transcriptional hyper-reactivity of junb. Using transfection and pharmacological assays to complement chromatin immunoprecipitation analyses addressing the localization of histones, polymerase II, negative elongation factor (NELF)-, DRB sensitivity-inducing factor (DSIF)- and Positive Transcription Factor b complexes, we demonstrate that junb is a RNA Pol II-paused gene where Pol II is loaded in the transcription start site domain but poorly active. Moreover, High salt-Recovered Sequence, chromosome conformation capture (3C)- and gene transfer experiments show that (i) junb is organized in a nuclear chromatin loop bringing into close spatial proximity the upstream promoter region and the downstream enhancer and (ii) this configuration permits immediate Pol II release on the junb body on binding of LPS-activated NF-κB to the enhancer. Thus, our work unveils a novel topological framework underlying fast junb transcriptional response in DCs. Moreover, it also points to a novel layer of complexity in the modes of action of NF-κB.
junb 基因在细菌脂多糖 (LPS) 刺激的树突状细胞 (DC) 中表现为即时早期基因,其瞬时转录激活对于诱导炎症细胞因子是必要的。junb 是一个短基因,其 LPS 转录激活依赖于 NF-κB 与位于其 3'UTR 下游的增强子结合。在这里,我们研究了 junb 转录过度反应的机制。通过转染和药理学测定来补充染色质免疫沉淀分析,以确定组蛋白、聚合酶 II、负延伸因子 (NELF)-、DRB 敏感性诱导因子 (DSIF)-和正转录因子 b 复合物的定位,我们证明 junb 是一个 RNA Pol II 暂停基因,其中 Pol II 加载在转录起始位点域,但活性较差。此外,高盐回收序列、染色体构象捕获 (3C) 和基因转移实验表明:(i) junb 组织在核染色质环中,将上游启动子区域和下游增强子紧密空间接近;(ii) 这种构象允许 LPS 激活的 NF-κB 与增强子结合后,Pol II 立即在 junb 主体上释放。因此,我们的工作揭示了 DC 中 junb 快速转录反应的新的拓扑结构框架。此外,它还指出了 NF-κB 作用模式的新的复杂性层次。