Wound repair in sea urchin larvae involves pigment cells and blastocoelar cells.

Sea urchin larvae spend weeks to months feeding on plankton prior to metamorphosis. When handled in the laboratory they are easily injured, suggesting that in the plankton they are injured with some frequency. Fortunately, larval wounds are repaired through an efficient wound response with mesenchymal pigment cells and blastocoelar cells assisting as the epithelium closes. An injury to the epithelium leads to an immediate calcium transient that rapidly spreads around the entire larva and is necessary for activating pigment cell migration toward the wound. If calcium transport is blocked, the pigment cells fail to activate and remain in place. When activated, pigment cells initiate directed migration to the wound site from distances of at least 85 â€‹µm. Upon arrival at the wound site they participate in an innate immune response. Blastocoelar cells are recruited to the injury site as well, though the calcium transient is unnecessary for activating these cells. At the wound site, blastocoelar cells participate in several functions including remodeling the skeleton if it protrudes through the epithelium.

Methods for transplantation of sea urchin blastomeres.

The stereotypic cleavage pattern of sea urchin embryos provides a platform for dissection of early lineage decisions that lead to cell diversification. Cell transplantation provides a useful tool for understanding those decisions. The methods described in this paper provide a guide for how to produce embryonic mosaics in which either one cell is transplanted or an entire tier of cells are transplanted to a host embryo. Although the results of such a cut and paste experiment can be documented in many ways, one of the most useful approaches follows progeny of the transplanted cell as they go through morphogenesis using time-lapse imaging. Methods for mounting and imaging the embryos are provided.