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Related Concept Videos

Chromatin Modification in iPS Cells01:32

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
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Related Experiment Video

Updated: Aug 14, 2025

A Simple Method to Identify Kinases That Regulate Embryonic Stem Cell Pluripotency by High-throughput Inhibitor Screening
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Changes in PRC1 activity during interphase modulate lineage transition in pluripotent cells.

Helena G Asenjo1,2,3, María Alcazar-Fabra1,2,3, Mencía Espinosa-Martínez1,2,3

  • 1Centre for Genomics and Oncological Research (GENYO), Avenue de la Ilustración 114, 18016, Granada, Spain.

Nature Communications
|January 12, 2023
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Summary

Pluripotent stem cells differentiate better in G1 phase due to cell cycle regulation. Polycomb Repressive Complex 1 (PRC1) activity increases in later phases, repressing differentiation genes until G1.

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Kinetic Measurement and Real Time Visualization of Somatic Reprogramming
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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Epigenetics

Background:

  • Pluripotent cells' differentiation potential varies across the cell cycle.
  • Molecular mechanisms linking cell cycle phase to differentiation gene regulation are unclear.
  • Polycomb group proteins are implicated in cell cycle-dependent gene expression.

Purpose of the Study:

  • To investigate the role of Polycomb Repressive Complex 1 (PRC1) in cell-cycle-regulated differentiation of pluripotent cells.
  • To elucidate how PRC1 activity changes during interphase and affects gene transcription.
  • To understand the preference for G1 phase in initiating differentiation gene activation.

Main Methods:

  • Assessed PRC1 recruitment and H2AK119 ubiquitination across cell cycle phases.
  • Analyzed 3D chromatin interactions during interphase.
  • Utilized genetic ablation of RING1B (PRC1 catalytic subunit) in mouse embryonic stem cells (mESCs).
  • Studied transcriptional activation of differentiation genes upon retinoic acid stimulation.

Main Results:

  • PRC1 recruitment and H2AK119 ubiquitination are higher in S and G2 phases than G1.
  • Cells in S and G2 phases exhibit stronger repression of developmental genes, dependent on PRC1's RING1B.
  • Depletion of RING1B disrupts the G1-phase preference for differentiation gene activation in mESCs.
  • Increased polycomb activity during interphase progression limits response to developmental cues in S/G2 phases.

Conclusions:

  • PRC1 activity incrementally increases during interphase, leading to enhanced repression of differentiation genes in S and G2 phases.
  • This cell-cycle-dependent repression facilitates the preferential activation of differentiation genes in the G1 phase.
  • The findings reveal a mechanism for cell-cycle-regulated differentiation in pluripotent stem cells.