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相关概念视频

Co-activators and Co-repressors02:04

Co-activators and Co-repressors

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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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Co-activators and Co-repressors02:04

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Cooperative Binding of Transcription Regulators02:13

Cooperative Binding of Transcription Regulators

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Transcriptional regulators bind to specific cis-regulatory sequences in the DNA to regulate gene transcription. These cis-regulatory sequences are very short, usually less than ten nucleotide pairs in length. The short length means that there is a high probability of the exact same sequence randomly occurring throughout the genome.  Since regulators can also bind to groups of similar sequences, this further increases the chances of random binding. Transcriptional regulators form...
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Cooperative Binding of Transcription Regulators02:13

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RNA Polymerase II Accessory Proteins02:36

RNA Polymerase II Accessory Proteins

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Proteins that regulate transcription can do so either via direct contact with RNA Polymerase or through indirect interactions facilitated by adaptors, mediators, histone-modifying proteins, and nucleosome remodelers. Direct interactions to activate transcription is seen in bacteria as well as in some eukaryotic genes. In these cases, upstream activation sequences are adjacent to the promoters, and the activator proteins interact directly with the transcriptional machinery. For example, in...
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RNA Polymerase II Accessory Proteins02:36

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相关实验视频

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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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转录调节器与核细胞相竞争

Srinivas Ramachandran1, Steven Henikoff1

  • 1Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA; Howard Hughes Medical Institute, Seattle, WA 98109, USA.

Cell
|April 12, 2016
PubMed
概括

在DNA复制后通过转录因子,RNA聚合酶II和重塑剂的作用恢复染色体组织. 这项研究揭示了核体的景观如何在复制后几分钟重新出现.

科学领域:

  • 分子生物学
  • 遗传学
  • 表观遗传学

背景情况:

  • DNA复制需要核体破坏和改造.
  • 复制后的染色体恢复机制尚不清楚.

研究的目的:

  • 研究DNA复制后全基因组染色体组织如何重新建立.
  • 描述复制叉背后的核细胞和蛋白质位置.

主要方法:

  • 使用EDU和测序 (MINCE-seq) 在体内绘制新生染色体.
  • MINCE-seq提供高时间和空间分辨率的染色体复制后.

主要成果:

  • 复制破坏了Drosophila促进剂和增强剂的特征性染色体格局.
  • 在促进体的高RNAPII停滞和DNA可访问性与BRM重塑剂丰富相关.
  • 增强色素破坏表明TF在核细胞重建中的竞争.

结论:

  • 这项研究阐明了复制后核格局的快速重新出现.
  • 转录因子,RNAPII和重塑剂是恢复色素组织的关键因素.
  • 一个均包装的基因组在复制几分钟后转变为特征景观.

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