小鼠和人类细胞中 NF-Y 的基因组结合。

IF 3.4 2区 生物学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
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引用次数: 0

摘要

NF-Y 是一种转录因子,它通过与 CCAAT-box 结合来调节转录。为了了解它的策略,我们分析了来自人类和小鼠细胞的 16 个 ChIP-seq 数据集。共享位点大多位于细胞周期、新陈代谢和基因表达途径中表达基因的启动子,与活跃染色质的组蛋白标记和特定的 TF 模块相关。其他峰值出现在人和小鼠的增强子和逆转录病毒源的可转座元件(Transposable Elements -TE)中。我们评估了 NF-YB 失活后与 USF1 的关系,USF1 是启动子和 MLT1 TEs 中常见的协同伙伴:USF1 与启动子的结合减少,而与 MLT1 的结合则适度减少,这表明 NF-Y 在启动子中起着先驱作用,而不是在后者中。这些数据确定了不同哺乳动物细胞类型中一组共同的 NF-Y 功能靶标,表明 NF-Y 在启动子中相对于 TEs 起着先驱作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Genomic binding of NF-Y in mouse and human cells

NF-Y is a Transcription Factor that regulates transcription through binding to the CCAAT-box. To understand its strategy, we analyzed 16 ChIP-seq datasets from human and mouse cells. Shared loci, mostly located in promoters of expressed genes of cell cycle, metabolism and gene expression pathways, are associated with histone marks of active chromatin and specific modules of TFs. Other peaks are in enhancers and Transposable Elements -TE- of retroviral origin in human and mouse. We evaluated the relationship with USF1, a common synergistic partner in promoters and MLT1 TEs, upon NF-YB inactivation: USF1 binding decreases in promoters, modestly in MLT1, suggesting a pioneering role of NF-Y in formers, not in the latters. These data define a common set of NF-Y functional targets across different mammalian cell types, suggesting a pioneering role in promoters with respect to TEs.

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来源期刊
Genomics
Genomics 生物-生物工程与应用微生物
CiteScore
9.60
自引率
2.30%
发文量
260
审稿时长
60 days
期刊介绍: Genomics is a forum for describing the development of genome-scale technologies and their application to all areas of biological investigation. As a journal that has evolved with the field that carries its name, Genomics focuses on the development and application of cutting-edge methods, addressing fundamental questions with potential interest to a wide audience. Our aim is to publish the highest quality research and to provide authors with rapid, fair and accurate review and publication of manuscripts falling within our scope.
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