Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET–Partner Institute of the Max Planck Society, Buenos Aires, Argentina; Departamento de Fisica, FCEyN, UBA, Ciudad Universitaria, Buenos Aires, Argentina; Department of Systemic Cell Biology, Max Planck Institute for Molecular Physiology, Dortmund, Germany
The Francis Crick Institute, London, United Kingdom; Department of Cell and Developmental Biology, University College London, London, United Kingdom; Institute of Bioengineering, École Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland
Segmentation of the axial skeleton in amniotes depends on the segmentation clock, which patterns the paraxial mesoderm and the sclerotome. While the segmentation clock clearly operates in teleosts, the role of the sclerotome in establishing the axial skeleton is unclear. We severely disrupt zebrafish paraxial segmentation, yet observe a largely normal segmentation process of the chordacentra. We demonstrate that axial entpd5+ notochord sheath cells are responsible for chordacentrum mineralization, and serve as a marker for axial segmentation. While autonomous within the notochord sheath, entpd5 expression and centrum formation show some plasticity and can respond to myotome pattern. These observations reveal for the first time the dynamics of notochord segmentation in a teleost, and are consistent with an autonomous patterning mechanism that is influenced, but not determined by adjacent paraxial mesoderm. This behavior is not consistent with a clock-type mechanism in the notochord.