Microridge Morphogenesis in Epithelial Cells

Microridges are laterally extended, labyrinthine actin-rich protrusions that adorn the apical surface of squamous epithelial cells across vertebrates. They arise during epithelial differentiation and play key roles in mucous retention, membrane reservoir formation and resistance to mechanical stress. Morphogenesis of microridges is driven by coordinated actin polymerisation, branching and contractile forces in the apical cortex. Initially, nascent actin punctae nucleate via the Arp2/3 complex, which fosters branched filament networks. Subsequent elongation, fusion and pattern rearrangements are orchestrated by the dynamic interplay of actin-binding proteins, small GTPases and cortical myosin II activity. Polarity regulators restrict protrusion length and maintain pattern fidelity by segregating basolateral factors from the apical domain. Emerging evidence also implicates intermediate filaments and cytolinker proteins in stabilising and tuning microridge dimensions. Together, these processes generate the highly ordered, maze-like arrays essential for epithelial barrier function and surface homeostasis.

Research from Nature Portfolio

Recent studies have revealed that apical-basolateral polarity cues critically limit microridge elongation. One report demonstrated that antagonistic interactions between atypical protein kinase C (aPKC) and the basolateral determinant Lgl regulate actin polymerisation at the apical cortex, preventing premature fusion and excessive protrusion length. aPKC activity excludes Lgl from the apical domain, controls non-muscle myosin II recruitment and thereby fine-tunes microridge dimensions. Another investigation characterised the underlying F-actin architecture using advanced microscopy and showed that microridges form a branched network reliant on continuous Arp2/3 activity. Pharmacological inhibition of actin polymerisation or Arp2/3 impaired microridge maintenance and disrupted the overlying glycan layer, highlighting their role in organising surface mucins.

Microridge Morphogenesis in Epithelial Cells publication trend

The graph below shows the total number of articles in microridge morphogenesis in epithelial cells across all publications each year (not limited to Nature Index journals).

Technical terms

Microridge: A laterally extended, actin-rich protrusion on the apical surface of squamous epithelial cells that forms a maze-like pattern.

Actomyosin network: A contractile system of actin filaments and myosin motors that generates cortical tension and drives morphological remodelling.

Arp2/3 complex: A seven-subunit protein assembly that nucleates branched actin filament networks essential for the initiation of protrusive structures.

Non-muscle myosin II (NMII): A motor protein that binds actin filaments to produce contractile forces, regulating protrusion fission, fusion and pattern stability.

aPKC (atypical protein kinase C): A serine/threonine kinase that defines apical domain identity and modulates cytoskeletal regulators to constrain protrusion growth.

Lgl (Lethal giant larvae): A basolateral polarity protein that, when mislocalized to the apical cortex, promotes unchecked actin polymerisation and elongation of microridges.

References

1. aPKC regulates apical localization of Lgl to restrict elongation of microridges in developing zebrafish epidermis. Nature Communications (2016).
2. Microridges are apical epithelial projections formed of F-actin networks that organize the glycan layer. Scientific Reports (2019).
3. A deep learning framework for quantitative analysis of actin microridges. npj Systems Biology and Applications (2023).
4. Keratins and Plakin family cytolinker proteins control the length of epithelial microridge protrusions. eLife (2020).
5. Stochastic contraction of myosin minifilaments drives evolution of microridge protrusion patterns in epithelial cells. Molecular Biology of the Cell (2021).