2024/10/11 by Maik C. Bischoff, Jenevieve E. Norton, Mark Peifer · 1 voice
Biochemistry, Genetics and Molecular Biology · Neuroscience · #Antagonism #Axon Guidance and Neuronal Signaling #Biology #Cell biology #Cellular Mechanics and Interactions #Closure (psychology) #Genetics #Hippo pathway signaling and YAP/TAZ #Plexin #Political science #Receptor #Semaphorin
paper · pdf · doi:10.1101/2024.10.10.617649
published in bioRxiv (Cold Spring Harbor Laboratory) (Cold Spring Harbor Laboratory)
openalex publication_date 2024/10/11 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/14
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 new Drosophila testis-nascent-myotube-system allows dissection of contact-dependent migration in vivo at high resolution. Here, we describe a process driving gap-closure during migration: Contact-mesenchymalization via the axon guidance factor Plexin A. This is crucial for testis myotubes to migrate as a continuous sheet, allowing normal sculpting-morphogenesis. Cells must stay filopodial and dynamically ECM-tethered near cell-cell contacts to spread while collectively moving. Our data suggest Semaphorin 1B acts as a Plexin A antagonist, fine-tuning activation. Our data reveal a contact-dependent mechanism to maintain sheet-integrity during migration, driving organ-morphogenesis using a highly conserved pathway. This is relevant for understanding mesenchymal organ-sculpting and gap-closure in migratory contexts like angiogenesis.