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Updated: May 28, 2025

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Isolation and Culture of Neural Crest Cells from Embryonic Murine Neural Tube
Published on: June 2, 2012
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Prickle2 regulates apical junction remodeling and tissue fluidity during vertebrate neurulation
Miho Matsuda1, Sergei Y Sokol1
1Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
The Journal of Cell Biology
|February 14, 2025
Summary
Prickle2 (Pk2) enhances tissue fluidity by remodeling apical junctions in Xenopus embryos, promoting cell elongation essential for neural tube development and anteroposterior axis formation.
Area of Science:
- Developmental biology
- Cell biology
- Molecular biology
Background:
- Neural tube formation requires tissue fluidity and the planar cell polarity (PCP) pathway.
- Epithelial deformation during development depends on maintaining tissue integrity.
Purpose of the Study:
- To investigate the role of Prickle2 (Pk2) in regulating tissue fluidity during neural tube development.
- To elucidate the molecular mechanisms by which Pk2 influences tissue properties and cell orientation.
Main Methods:
- Utilized Xenopus embryos as a model system.
- Investigated the function of Prickle2 (Pk2) and its Ser/Thr-rich region (STR).
- Analyzed the involvement of Rac1, C-cadherin, and tricellular junctions.
Main Results:
- Pk2 increases tissue fluidity by promoting apical junction (AJ) remodeling.
- Pk2's function is mediated by its STR and requires Rac1.
- Pk2 depletion causes mediolateral cell orientation; Pk2 overexpression promotes anteroposterior cell elongation.
Conclusions:
- Pk2 regulates tissue fluidity through AJ dynamics, impacting cell shape and tissue elongation.
- Pk2-dependent tissue fluidity is crucial for anteroposterior axis formation in response to developmental cues.
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