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Patterned integrin-laminin adhesion coordinates epithelial collective cell migration

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Collective cell migration is essential for development, tissue homeostasis, and disease progression. Although integrin-mediated adhesion is well characterized in single migrating cells in vitro, how integrins coordinate collective epithelial migration in vivo is less clear. Using the zebrafish posterior lateral line primordium (pLLP), we show that integrins α3 and α6 are differentially expressed in the trailing and leading regions of the pLLP, respectively, and that their combined loss induces excessive protrusive activity and slows migration. We further identify laminin α5 (Lama5) as a key basement membrane (BM) component underlying migrating pLLP cells. While loss of laminin α5 alone compromises BM integrity without impairing migration, simultaneous depletion of lama5 and itga6b markedly decreases velocity, and ultimately blocks migration. These findings reveal a robust, redundant adhesion machinery that ensures persistent collective migration in vivo and highlight fundamental principles of epithelial dynamics relevant to development and disease.
Title: Patterned integrin-laminin adhesion coordinates epithelial collective cell migration
Description:
Collective cell migration is essential for development, tissue homeostasis, and disease progression.
Although integrin-mediated adhesion is well characterized in single migrating cells in vitro, how integrins coordinate collective epithelial migration in vivo is less clear.
Using the zebrafish posterior lateral line primordium (pLLP), we show that integrins α3 and α6 are differentially expressed in the trailing and leading regions of the pLLP, respectively, and that their combined loss induces excessive protrusive activity and slows migration.
We further identify laminin α5 (Lama5) as a key basement membrane (BM) component underlying migrating pLLP cells.
While loss of laminin α5 alone compromises BM integrity without impairing migration, simultaneous depletion of lama5 and itga6b markedly decreases velocity, and ultimately blocks migration.
These findings reveal a robust, redundant adhesion machinery that ensures persistent collective migration in vivo and highlight fundamental principles of epithelial dynamics relevant to development and disease.

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