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SUMMARY:Maik Bischoff-Plexin/Semaphorin Antagonism Orchestrates Collective
  Cell Migration and Organ Sculpting by Regulating Epithelial-Mesenchymal B
 alance\; Harry McNamara-Decoding and controlling self-organization in stem
  cell models of embryonic development - Maik Christian Bischoff\, UNC\, Ma
 rk Peifer lab\; Harry McNamara\, Yale University
DTSTART:20250602T133000Z
DTEND:20250602T143000Z
UID:TALK230869@talks.cam.ac.uk
CONTACT:Jia CHEN
DESCRIPTION:Maik Christian Bischoff \n\nTitle: Plexin/Semaphorin Antagonis
 m Orchestrates Collective Cell Migration and Organ Sculpting by Regulating
  Epithelial-Mesenchymal Balance \n\nAbstract:Cell behavior emerges from th
 e intracellular distribution of properties like protrusion\, contractility
 \, and adhesion. Thus\, characteristic emergent rules of collective migrat
 ion can arise from cell-cell contacts locally tweaking architecture\, orch
 estrating self-regulation during development\, wound healing\, and cancer 
 progression. The Drosophila testis-nascent-myotube-system allows disse
 ction 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 epit
 helial-mesenchymal spectrum. This is crucial for testis myotubes to migrat
 e as a continuous sheet\, allowing normal sculpting-morphogenesis. Cells m
 ust maintain filopodial N-cadherin-based junctions and remain ECM-tethered
  near cell-cell contacts to spread while collectively moving. Our data fur
 ther suggest Semaphorin 1b is a Plexin A antagonist\, fine-tuning activati
 on. This reveals a contact-dependent mechanism to maintain sheet-integrity
  during migration\, driving organ-morphogenesis. This is relevant for mese
 nchymal organ-sculpting in other migratory contexts like angiogenesis. \n\
 nHarry McNamara (Assistant Professor of Molecular\, Cellular and Developme
 ntal Biology\, Yale University) \n\nTitle: Decoding and controlling self-o
 rganization in stem cell models of embryonic development \n\nAbstract: The
  arrival of stem cell-based models of embryonic development (organoids\, g
 astruloids\, embryo models) presents new opportunities to investigate mult
 icellular self-organization. Although development is often studied as a to
 p-down process in which external spatial cues (such as morphogen gradients
 ) instruct cell fate decisions\, it is also thought that internal feedback
 s in signaling networks can self-organize pattern formation from the botto
 m-up. Stem cell models use self-organization to generate cell types and ti
 ssue structures which resemble those built by real embryos. Despite rapid 
 advances in stem cell model complexity and detailed comparisons to their i
 n vivo counterparts\, we have a comparatively limited understanding of how
  they emerge from cell signaling interactions. Unlocking the full potentia
 l of stem cell models will require not only characterizing their outputs b
 ut also understanding how they work. \n\nWe investigate stem cell self-org
 anization by programming cells to read and write morphogen signals. By pro
 gramming cells to record signaling activity\, we can link early cell state
 s to future cell fates and decode the origins of pattern formation. By con
 trolling cell signaling with optogenetics\, we can re-introduce spatial cu
 es into stem cell models to guide morphogenesis and test predictions of qu
 antitative theories. We will describe recent work applying this approach t
 o study anterior-posterior symmetry breaking in the gastruloid as well as 
 future opportunities in other stem cell developmental models. 
LOCATION:Online
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