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Updated: Jun 9, 2025

Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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H3K27 dimethylation dynamics reveal stepwise establishment of facultative heterochromatin in early mouse embryos

Masahiro Matsuwaka1,2, Mami Kumon1, Azusa Inoue3,4

  • 1Laboratory for Epigenome Inheritance, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.

Nature Cell Biology
|November 1, 2024
PubMed

Insights

Facultative heterochromatin establishment involves Polycomb repressive complex 2 (PRC2) and PRC1. This study reveals PRC2.2-driven H3K27 methylation follows H2AK119ub1 deposition during early embryogenesis.

Area of Science:

  • Epigenetics
  • Developmental Biology
  • Genomics

Background:

  • Facultative heterochromatin formation relies on H3K27me3 (PRC2) and H2AK119ub1 (PRC1).
  • The precise mechanism of facultative heterochromatin establishment post-fertilization is not fully understood.

Purpose of the Study:

  • To investigate the temporal dynamics and establishment kinetics of facultative heterochromatin during mouse preimplantation development.
  • To elucidate the role of JARID2 in the de novo deposition of H3K27 methylation.

Main Methods:

  • Profiling temporal dynamics of H3K27me2 in mouse preimplantation embryos.
  • Investigating the colocalization of JARID2 and SUZ12.
  • Analyzing the impact of JARID2 depletion on histone modifications and PRC2 binding.

Main Results:

  • H3K27me2 deposition occurs at CpG islands, the paternal X chromosome, and enhancers during the eight-cell to morula transition, following H2AK119ub1.
  • JARID2 binds to H2AK119ub1 and colocalizes with SUZ12 at specific genomic loci.
  • JARID2 depletion impairs SUZ12 binding, H3K27me2 deposition, and leads to increased H3K27 acetylation, ultimately inhibiting H3K27me3 formation.

Conclusions:

  • Facultative heterochromatin is established through a stepwise process driven by PRC2.2.
  • H3K27 methylation is guided by pre-deposited H2AK119ub1 during early embryogenesis.
  • JARID2 plays a crucial role in recruiting PRC2 to target sites for de novo heterochromatin formation.

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