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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
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Modeling Paracrine Noncanonical Wnt Signaling In Vitro
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Bivalent Histone Codes on WNT5A during Odontogenic Differentiation.

Y Zhou1, L Zheng1, F Li1

  • 11 State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Journal of Dental Research
|September 8, 2017
PubMed
Summary
This summary is machine-generated.

Epigenetic regulation of WNT5A by H3K4me3 and H3K27me3 marks, mediated by JMJD3 and MLL complexes, controls odontogenic differentiation and lineage commitment.

Keywords:
KDM6BMLL proteindental papillaepigeneticsgene expressionhistone modifications

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Area of Science:

  • Epigenetics
  • Developmental Biology
  • Molecular Biology

Background:

  • Lineage-committed differentiation during odontogenesis is crucial for tooth development.
  • Bivalent domains (H3K4me3/H3K27me3) poise genes for differentiation.
  • WNT5A promotes odontogenic differentiation, but its epigenetic regulation is unclear.

Purpose of the Study:

  • Investigate spatiotemporal patterns of H3K4me3 and H3K27me3 during tooth development.
  • Elucidate the role of epigenetic modifiers (JMJD3, UTX, MLL complex) in WNT5A regulation.
  • Determine how epigenetic modifications influence odontogenic commitment.

Main Methods:

  • Analysis of H3K4me3 and H3K27me3 marks in developing mouse molars and human dental papilla cells (hDPCs).
  • Assessment of methylase (MLL complex) and demethylase (JMJD3, UTX) expression during odontogenic induction.
  • Gene knockdown experiments (JMJD3) in hDPCs to assess effects on differentiation and WNT5A activation.
  • Co-immunoprecipitation to investigate protein interactions (JMJD3 and ASH2L).

Main Results:

  • WNT5A promoters exhibit bivalent domains (H3K4me3/H3K27me3) in poised progenitor cells.
  • JMJD3-dependent removal of H3K27me3 resolves bivalent domains during differentiation.
  • JMJD3 knockdown suppresses odontogenic differentiation and WNT5A activation by increasing H3K27me3.
  • JMJD3 interacts with MLL complex component ASH2L to modulate H3K4me3.

Conclusions:

  • WNT5A transcription is epigenetically controlled by the balance of H3K27me3 and H3K4me3 marks.
  • JMJD3 and the MLL coactivator complex are key mediators of WNT5A epigenetic regulation.
  • This epigenetic mechanism tightly regulates odontogenic commitment during dental mesenchymal differentiation.