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转录激活因子与沉默基因座的结合导致它们在神经元和唾液腺细胞中从核纤层脱离。

Binding of Transcriptional Activator to Silent Loci Causes Their Detachment from the Nuclear Lamina in Neurons and Salivary Gland Cells.

作者信息

Simonov Ruslan A, Olenkina Oxana M, Nenasheva Valentina V, Abramov Yuri A, Lavrov Sergey A, Fedotova Anna A, Shevelyov Yuri Y

机构信息

Laboratory of Analysis of Gene Regulation, National Research Centre "Kurchatov Institute", 123182 Moscow, Russia.

Laboratory of Molecular Neurogenetics and Innate Immunity, National Research Centre "Kurchatov Institute", 123182 Moscow, Russia.

出版信息

Int J Mol Sci. 2025 Jun 17;26(12):5793. doi: 10.3390/ijms26125793.

Abstract

In mammals, the binding of transcriptional activators leads to the repositioning of silent loci from the nuclear periphery to the nuclear interior. However, it remained unknown whether the same mechanism functions in . Here, using FISH and DamID, we have shown that binding the GAL4 activator to the silent loci causes weakening of their interactions with the nuclear lamina and relocalization inside nuclei in salivary gland cells and neurons. This mimics the removal from the nuclear periphery of a neuron-specific gene upon its activation in neurons. Salivary gland cells contain polytene chromosomes with mechanical properties, different from chromosomes of diploid cells, while neurons represent predominantly non-dividing cell type. Our results indicate a causal relationship between transcriptional activator binding and changes in the intranuclear position of loci in . They also point to the similarity in general chromatin dynamics in mammals and , thus strengthening the role of model organisms in studying genome architecture.

摘要

在哺乳动物中,转录激活因子的结合会导致沉默基因座从核周边重新定位到核内部。然而,在[具体生物]中是否存在相同机制仍不清楚。在这里,我们使用荧光原位杂交(FISH)和DNA腺嘌呤甲基转移酶识别测序(DamID)技术表明,在唾液腺细胞和神经元中,将GAL4激活因子与沉默基因座结合会导致它们与核纤层的相互作用减弱,并在细胞核内重新定位。这模拟了神经元特异性基因在神经元中被激活后从核周边移除的过程。唾液腺细胞含有具有机械特性的多线染色体,与二倍体细胞的染色体不同,而神经元主要代表非分裂细胞类型。我们的结果表明转录激活因子结合与[具体生物]中基因座核内位置变化之间存在因果关系。它们还指出了哺乳动物和[具体生物]在一般染色质动力学方面的相似性,从而加强了模式生物在研究基因组结构中的作用。

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