A morphogenetic EphB/EphrinB code controls hepatopancreatic duct formation
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Authors
Thestrup, MICaviglia, S
Cayuso, J
Heyne, RLS
Ahmad, R
Hofmeister, W
Satriano, L
Wilkinson, DG
Andersen, JB
Ober, EA
Issue Date
2019-11-19
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Show full item recordAbstract
The hepatopancreatic ductal (HPD) system connects the intrahepatic and intrapancreatic ducts to the intestine and ensures the afferent transport of the bile and pancreatic enzymes. Yet the molecular and cellular mechanisms controlling their differentiation and morphogenesis into a functional ductal system are poorly understood. Here, we characterize HPD system morphogenesis by high-resolution microscopy in zebrafish. The HPD system differentiates from a rod of unpolarized cells into mature ducts by de novo lumen formation in a dynamic multi-step process. The remodeling step from multiple nascent lumina into a single lumen requires active cell intercalation and myosin contractility. We identify key functions for EphB/EphrinB signaling in this dynamic remodeling step. Two EphrinB ligands, EphrinB1 and EphrinB2a, and two EphB receptors, EphB3b and EphB4a, control HPD morphogenesis by remodeling individual ductal compartments, and thereby coordinate the morphogenesis of this multi-compartment ductal system.Citation
hestrup, M.I., Caviglia, S., Cayuso, J. et al. (2019) A morphogenetic EphB/EphrinB code controls hepatopancreatic duct formation. Nat Commun 10, 5220. https://doi.org/10.1038/s41467-019-13149-7Publisher
Springer Science and Business Media LLCJournal
Nature CommunicationsPubMed ID
31745086 (pubmed)Additional Links
https://www.nature.com/articles/s41467-019-13149-7Type
Journal articleLanguage
enDescription
© 2019 The Authors. Published by Springer. This is an open access article available under a Creative Commons licence. The published version can be accessed at the following link on the publisher’s website: https://doi.org/10.1038/s41467-019-13149-7ISSN
2041-1723EISSN
2041-1723Sponsors
This work was funded by the Novo Nordisk Foundation (NNF17CC0027852) and Danish National Research Foundation (DNRF116). J.C. and D.G.W. were supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK (FC001217), the UK Medical Research Council (FC001217), and the Wellcome Trust (FC001217). S.C. was supported by an SNSF Early Postdoc Mobility fellowship (P2ZHP3_164840) and a Long Term EMBO Postdoc fellowship (ALTF 511-2016), and L.S. and J.B.A. by the Independent Research Fund Denmark (DFF; Sapere Aude2 4183-00118B).ae974a485f413a2113503eed53cd6c53
10.1038/s41467-019-13149-7
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Except where otherwise noted, this item's license is described as Licence for published version: Creative Commons Attribution 4.0 International
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