Expression and Transcriptional Targets of TGFβ-RII in Paracentrotus lividus Larval Skeletogenesis

Organisms from the five kingdoms of life use minerals to harden their tissues and make teeth, shells and skeletons, in the process of biomineralization. The sea urchin larval skeleton is an excellent system to study the biological regulation of biomineralization and its evolution. The gene regulatory network (GRN) that controls sea urchin skeletogenesis is known in great details and shows similarity to the GRN that controls vertebrates' vascularization while it is quite distinct from the GRN that drives vertebrates' bone formation. Yet, transforming growth factor beta (TGF-β) signaling regulates both sea urchin and vertebrates' skeletogenesis. Here, we study the upstream regulation and identify transcriptional targets of TGF-β in the Mediterranean Sea urchin species, Paracentrotus lividus. TGF-βRII is transiently active in the skeletogenic cells downstream of vascular endothelial growth factor (VEGF) signaling, in P. lividus. Continuous perturbation of TGF-βRII activity significantly impairs skeletal elongation and the expression of key skeletogenic genes. Perturbation of TGF-βRII after skeletal initiation leads to a delay in skeletal elongation and minor changes in gene expression. TGF-β targets are distinct from its transcriptional targets during vertebrates' bone formation, suggesting that the role of TGF-β in biomineralization in these two phyla results from convergent evolution.