How does Astacin-4 regulate the epithelial-mesenchymal transition of urchin immune cells during embryonic development?

Zach Pracher

Mentor: Dave McClay, Ph.D.

Department of Biology

The developmental gene regulatory network (GRN) of the green sea urchin (Lytechinus variegatus) has been extensively investigated to illuminate the genetic interactions underlying embryonic development and has led to many insights in embryonic development and regeneration. Although the putative metalloprotease Astacin-4 is widely expressed in urchin embryonic blastocoelar cells, its developmental function and position in the established developmental GRN remains unknown. In our study, inhibiting Nodal with an antagonistic drug throughout embryonic development revealed that Nodal signaling between 4 and 6 hours post fertilization is critical to downstream Astacin-4 expression, blastocoelar cell formation, and overall embryo development. Separately, we repressed Astacin-4 expression using a morpholino to determine the potential role of Astacin-4 in embryonic and blastocoelar development and function. Embryo morphology and gene expression patterns were subsequently assessed using in situ hybridization and microscopy techniques. We hypothesize that repressing Astacin-4 inhibits normal blastocoelar cell formation, and we generally expect to elucidate the role of Astacin-4 in the epithelial-mesenchymal transition of blastocoelar cell precursors. Understanding the regulation and function of Astacin-4 in L. variegatus can enhance our knowledge of the genetic relationships underlying immune system development as well as evolutionary conservation of immune system development across the animal kingdom.

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