The findings suggest that BMP ligands are released from these micromere derived skeletogenic cells to regulate LR asymmetry. It was previously found that when the micromere lineage was taken from embryos of sea urchin Hemicentrotus pulcherrimus, the LR placement of the rudiment was randomized. e3 ubiquitin BMP could be the micromerederived signal that regulates larval LR polarity, though other signaling molecules may also be associated with this process. People from Smm removed embryos produced little gonads without gametes. Consequently, Smm are expected for germline specification in sea urchins. Smm lineage fate is preserved by Nanos, which will be also required for Smm descendant survival. Studies in vertebrates and fly also have found that Nanos has a conserved role in keeping germline identity by preventing apoptosis. In this study, we showed that Nodal signaling functions to the Smm partitioned in the CP. Nodal signaling perturbation affected both nanos2 Eumycetoma expression and cell death. These results suggest that Nodal signaling in the right CP represses nanos2 appearance in the Smm, which leads to cell death. To the knowledge, the part of Nodal signaling in repressing the expression of germline lineage genes for example nanos hasn’t been reported in other systems. Intriguingly, Nodal is capable of inducing apoptosis in ovary during follicular degeneration and human trophoblast cells during normal placentation. For that reason, there might be a role for Nodal natural product libraries to induce apoptosis in extraembryonic tissues. In case of sea urchins, Nodal signaling induced apoptosis within the right Smm is important for normal development, and a lack of Nodal results in bilateral rudiments that give rise to a juvenile composed of two conjoined urchins. Materials and Practices Animals, Embryos, and Treatments Adult sea urchins and their gametes were obtained as previously described. Rhodomonas contact provided by Pat Leahy was used to feed the larva. BMP or Nodal signaling perturbation was performed by treating embryos with inhibitors, recombinant proteins, or vivo morpholinos and culturing them in the dark. Unless otherwise indicated, the concentrations of the reagents utilized in this study were as mouse BMP4, SB 431542, SB 505124, follows: dorsomorphin, and human Activin AB. Solvents were added as controls. The sequences of the BMP and Nodal vMOs are the same as the previously published typical MOs. vMOs were diluted at 1:100 to 5 mM from stock solution in phosphate buffered saline into 500 ml of culture. The procedure times are described in Figures S3H and S4E.