Chordacentrum mineralization is delayed in zebrafish betaglycan-null mutants

Background The Transforming Growth Factor beta (TGF beta) family is a group of related proteins that signal through a type I and type II receptors. Betaglycan, also known as the type III receptor (Tgfbr3), is a coreceptor for various ligands of the TGF beta family that participates in heart, liver and kidney development as revealed by the tgfbr3-null mouse, as well as in angiogenesis as revealed by Tgfbr3 downregulation in morphant zebrafish. Results Here, we present CRISPR/Cas9-derived zebrafish Tgfbr3-null mutants, which exhibited unaltered embryonic angiogenesis and developed into fertile adults. One reproducible phenotype displayed by these Tgfbr3-null mutants is delayed chordacentra mineralization, which nonetheless does not result in vertebral abnormalities in the adult fishes. We also report that the canonical TGF beta signaling pathway is needed for proper chordacentra mineralization and that Tgfbr3 absence decreases this signal in the notochordal cells responsible for this process. Conclusion Betaglycan's ligand presentation function contributes to the optimal TGF beta signaling required for zebrafish chordacentra mineralization.

Automated summary

In this study, zebrafish Tgfbr3-null mutants were generated using CRISPR/Cas9 technology. The mutants showed unaltered embryonic angiogenesis and developed into fertile adults. A consistent phenotype in these mutants was delayed chordacentra mineralization, which did not lead to vertebral abnormalities in adult fishes.