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Related Concept Videos

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Certain biochemical processes, such as embryonic development and cell growth regulation, depend on the repression of specific genes. DNA binding proteins known as eukaryotic transcription inhibitors regulate the repression of gene expression in eukaryotes. The presence of these inhibitors at the required location and time in the cell is triggered by the presence of hormones and additional signals from other cells.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Related Experiment Video

Updated: Aug 5, 2025

A Method to Study de novo Formation of Chromatin Domains
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PR-DUB safeguards Polycomb repression through H2AK119ub1 restriction.

Rui Li1, Dandan Huang2, Yingying Zhao1

  • 1State Key Laboratory of Experimental Hematology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Cell Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.

Cell Proliferation
|March 24, 2023
PubMed
Summary
This summary is machine-generated.

Polycomb repressive deubiquitinase (PR-DUB) restricts histone H2AK119ub1, ensuring Polycomb repressive complex 1 (PRC1) binding. PR-DUB deficiency disrupts PRC1 deposition, impairing gene silencing and cell fate control.

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Area of Science:

  • Epigenetics
  • Chromatin biology
  • Developmental biology

Background:

  • Polycomb group (PcG) proteins regulate cell fate via chromatin modification.
  • Histone H2AK119 mono-ubiquitylation (H2AK119ub1) is mediated by Polycomb repressive complex 1 (PRC1) for transcription repression.
  • The Polycomb repressive deubiquitinase (PR-DUB) complex, including BAP1 and ASXL proteins, removes H2AK119ub1, but its role in PcG silencing remains unclear.

Purpose of the Study:

  • To investigate the function of PR-DUB in regulating H2AK119ub1 distribution and its impact on PcG silencing.
  • To determine how PR-DUB deficiency affects chromatin states and gene expression in mouse embryonic stem cells (ESCs).

Main Methods:

  • Epigenomic analysis in Asxl2-deficient mouse ESCs.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to assess PRC1 occupancy and H2AK119ub1 levels.
  • Gene expression analysis before and after lineage differentiation.

Main Results:

  • H2AK119ub1 is generally distributed away from promoters and positively correlates with PRC1 occupancy.
  • Deletion of Asxl2 leads to increased H2AK119ub1 genome-wide and enhanced PRC1 sampling.
  • PRC1 is lost from a subset of highly occupied promoters in Asxl2-null ESCs, causing impaired gene silencing during differentiation.

Conclusions:

  • Genome-wide restriction of H2AK119ub1 by PR-DUB is crucial for maintaining proper PRC1 deposition at target genes.
  • PR-DUB activity is essential for robust PcG-mediated gene silencing and normal developmental regulation.