This research demonstrates how laminin α5 and integrin α6b coordinate for polarity maintenance in zebrafish epidermis, suggesting a shared pathway.
Polarity is one of the fundamental properties of cells. It is characterised by the asymmetric distribution of lipids and proteins in the cell membrane and cortex, and organelles in the cell. Cell polarisation drives essential processes such as morphogenesis, cell migration, asymmetric cell division, directional transport of molecules across epithelium, nerve impulse transmission etc. Although, the importance of polarity proteins such as atypical protein kinase C (aPKC) and Lgl2 (lethal giant larvae 2) has been relatively well understood in the developing zebrafish epidermis, whether basal lamina components are important for polarity maintenance has remained unclear. I analysed the role of Lamininα5 (basal lamina component) in the establishment and maintenance of apicobasal polarity, in developing bi-layered zebrafish epidermis. I found that the loss of laminin α5 function results in reduced E-cadherin localization and increased cell spreading along with dynamic cell boundaries and increased cell proliferation indicating acquisition of mesenchymal traits. A similar phenotype was observed in integrin α6b mutant, which did not exacerbate in the double mutant embryos indicating that laminin α5 and integrin α6b function in the same pathway. Interestingly, periderm, the cell layer above basal epidermis, maintains its apicobasal polarity and epithelial integrity presumably via reinforcing the localization of aPKC and Lgl. My work unravels the importance of Laminin α5 and Integrin α6b interaction in the maintenance of epithelial characteristics in the basal layer of the developing zebrafish epidermis.
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Tooba Khan (2025) studied this question.
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