期刊
DEVELOPMENTAL BIOLOGY
卷 491, 期 -, 页码 56-65出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2022.08.005
关键词
Larval wound repair; Skeletal remodeling; Pigment cell motility
资金
- NIH [RO1 HD14483, T32HD040372]
- NSF [GRFP 1644868]
- NIH NIGMS [R35127059]
Sea urchin larvae have an efficient wound response mechanism, involving pigment cells and blastocoelar cells. Calcium transient is triggered upon injury, activating pigment cells and recruiting blastocoelar cells for repair.
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 to-ward 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 ??m. 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.
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