University of Cambridge > Talks.cam > Morphogenesis Seminar Series > Maik Christian Bischoff-Plexin/Semaphorin Antagonism Orchestrates Collective Cell Migration and Organ Sculpting by Regulating Epithelial-Mesenchymal Balance

Maik Christian Bischoff-Plexin/Semaphorin Antagonism Orchestrates Collective Cell Migration and Organ Sculpting by Regulating Epithelial-Mesenchymal Balance

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  • UserMaik Christian Bischoff, UNC, Mark Peifer lab; Harry McNamara
  • ClockMonday 02 June 2025, 14:30-15:30
  • HouseOnline.

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Maik Christian Bischoff

Title:

Plexin/Semaphorin Antagonism Orchestrates Collective Cell Migration and Organ Sculpting by Regulating Epithelial-Mesenchymal Balance

Abstract

Cell behavior emerges from the intracellular distribution of properties like protrusion, contractility, and adhesion. Thus, characteristic emergent rules of collective migration can arise from cell-cell contacts locally tweaking architecture, orchestrating self-regulation during development, wound healing, and cancer progression. The Drosophila testis-nascent-myotube-system allows dissection of contact-dependent migration in vivo at high resolution. Here, we describe a role for the axon guidance factor Plexin A in collective cell migration: maintaining cell-cell interfaces at a precise point on the epithelial-mesenchymal spectrum. This is crucial for testis myotubes to migrate as a continuous sheet, allowing normal sculpting-morphogenesis. Cells must maintain filopodial N-cadherin-based junctions and remain ECM -tethered near cell-cell contacts to spread while collectively moving. Our data further suggest Semaphorin 1b is a Plexin A antagonist, fine-tuning activation. This reveals a contact-dependent mechanism to maintain sheet-integrity during migration, driving organ-morphogenesis. This is relevant for mesenchymal organ-sculpting in other migratory contexts like angiogenesis.

This talk is part of the Morphogenesis Seminar Series series.

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