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Cultivating a Three-dimensional Reconstructed Human Epidermis at a Large Scale
Published on: May 28, 2021
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Meisosomes, folded membrane microdomains between the apical extracellular matrix and epidermis
Dina Aggad1, Nicolas Brouilly2, Shizue Omi1
1Aix Marseille Univ, INSERM, CNRS, CIML, Turing Centre for Living Systems, Marseille, France.
Elife
|March 13, 2023
Summary
Mutant worms lacking skin furrows lose connection between epidermis and cuticle. New structures called meisosomes, formed by plasma membrane folds, may connect lateral epidermis to cuticle and relay damage signals.
Area of Science:
- Cell biology
- Biophysics
- Developmental biology
Background:
- Apical extracellular matrices (aECMs) provide a crucial physical barrier.
- The nematode cuticle, an epidermal aECM, comprises collagens forming ridges and furrows.
- Epidermal connections to the cuticle are vital for skin integrity.
Purpose of the Study:
- Investigate the role of epidermal furrows in maintaining the connection between the epidermis and the cuticle.
- Characterize novel ultrastructural components in mutants lacking epidermal furrows.
- Explore the function of these structures in biomechanical signaling and damage response.
Main Methods:
- Electron microscopy to analyze ultrastructure in wild-type and mutant Caenorhabditis elegans.
- Biomechanical property assessment of mutant skin.
- Localization studies for phosphatidylinositol (4,5) bisphosphate.
Main Results:
- Mutants lacking furrows exhibit a loss of epidermal-cuticle connection, particularly at the lateral epidermis.
- Novel structures, termed meisosomes (stacked plasma membrane folds filled with cuticle), are identified.
- Meisosomes are associated with phosphatidylinositol (4,5) bisphosphate-enriched domains and may function in signal transduction.
Conclusions:
- Meisosomes are proposed to connect the lateral epidermis to the cuticle, analogous to hemidesmosomes elsewhere.
- Furrow mutants show altered skin biomechanics and constitutive epidermal damage response.
- Meisosomes may serve as signaling platforms relaying mechanical stress from the aECM to the epidermis.
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