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首页> 外文期刊>Journal of Molecular Biology >Cooperativeness of the higher chromatin structure of the beta-globin locus revealed by the deletion mutations of DNase I hypersensitive site 3 of the LCR
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Cooperativeness of the higher chromatin structure of the beta-globin locus revealed by the deletion mutations of DNase I hypersensitive site 3 of the LCR

机译：LCR的DNase I超敏位点3的缺失突变揭示了β-珠蛋白基因座较高染色质结构的协同性

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摘要

High-level transcription of the globin genes requires the enhancement by a distant element, the locus control region (LCR). Such long-range regulation in vivo involves spatial interaction between transcriptional elements, with intervening chromatin looping out. It has been proposed that the clustering of the HS sites of the LCR, the active globin genes, as well as the remote 5' hypersensitive sites (HSs) (HS-60/-62 in mouse, HS-110 in human) and 3'HS1 forms a specific spatial chromatin structure, termed active chromatin hub (ACH). Here we report the effects of the HS3 deletions of the LCR on the spatial chromatin structure of the beta-globin locus as revealed by the chromatin conformation capture (3C) technology. The small HS3 core deletion (0.23 kb), but not the large HS3 deletion (2.3 kb), disrupted the spatial interactions among all the HS sites of the LCR, the beta-globin gene and 3'HS1. We have previously demonstrated that the large HS3 deletion barely impairs the structure of the LCR holocomplex, while the structure is significantly disrupted by the HS3 core deletion. Taken together, these results suggest that the formation of the ACH is dependent on a largely intact LCR structure. We propose that the ACH indeed is an extension of the LCR holocomplex.
机译：珠蛋白基因的高水平转录需要通过一个遥远的元件-基因座控制区（LCR）-来增强。这种体内的远程调节涉及转录元件之间的空间相互作用，以及染色质的介入。已经提出，LCR的HS位点，活性球蛋白基因以及远端的5'超敏位点（HS）（小鼠中的HS-60 / -62，人中的HS-110）和3的聚类“ HS1形成特定的空间染色质结构，称为活性染色质集线器（ACH）。在这里我们报告了染色质构象捕获（3C）技术揭示的LCR的HS3缺失对β珠蛋白基因座的空间染色质结构的影响。较小的HS3核心缺失（0.23 kb），而不是较大的HS3缺失（2.3 kb），破坏了LCR，β-珠蛋白基因和3'HS1的所有HS位点之间的空间相互作用。我们以前已经证明，大的HS3缺失几乎不会损害LCR全息复合体的结构，而HS3核心缺失会显着破坏该结构。综上所述，这些结果表明ACH的形成取决于很大程度上完整的LCR结构。我们认为ACH确实是LCR全息复合体的扩展。

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