EphrinB1/EphB3b coordinate bidirectional epithelial-mesenchymal interactions controlling liver morphogenesis and laterality
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AbstractPositioning organs in the body often requires the movement of multiple tissues, yet the molecular and cellular mechanisms coordinating such movements are largely unknown. Here, we show that bidirectional signaling between EphrinB1 and EphB3b coordinates the movements of the hepatic endoderm and adjacent lateral plate mesoderm (LPM), resulting in asymmetric positioning of the zebrafish liver. EphrinB1 in hepatoblasts regulates directional migration and mediates interactions with the LPM, where EphB3b controls polarity and movement of the LPM. EphB3b in the LPM concomitantly repels hepatoblasts to move leftward into the liver bud. Cellular protrusions controlled by Eph/Ephrin signaling mediate hepatoblast motility and long-distance cell-cell contacts with the LPM beyond immediate tissue interfaces. Mechanistically, intracellular EphrinB1 domains mediate EphB3b-independent hepatoblast extension formation, while EpB3b interactions cause their destabilization. We propose that bidirectional short- and long-distance cell interactions between epithelial and mesenchyme-like tissues coordinate liver bud formation and laterality via cell repulsion.
CitationCayuso, J., Dzementsei, A., Fischer, J.C. et al. (2016) EphrinB1/EphB3b coordinate bidirectional epithelial-mesenchymal interactions controlling liver morphogenesis and laterality. Developmental Cell, 39(3), pp. 316-328.
PubMed ID27825440 (pubmed)
Description© 2016 The Authors. Published by Elsevier. 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/10.1016/j.devcel.2016.10.009
SponsorsThis work was funded by the Medical Research Council ( U117581329 ), Novo Nordisk Foundation ( NNF15CC0018344 ), Danish National Research Foundation ( DNRF116 ), Wellcome Trust ( 098051 ), and an Early Postdoc Mobility Fellowship from the Swiss National Science Foundation to S.C..
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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