Sea Urchin Embryo: Specification of Cell Fates

Abstract

Specification of cell fate in sea urchin embryos involves initial asymmetric distribution of maternal molecules that establish posterior and anterior domains of transcription activity. Subsequently, fates of most blastomeres along the anterior–posterior and dorsal–ventral axes of the embryo are patterned by cell–cell interactions involving signalling ligands and cell surface receptors. These signalling pathways regulate the operation of networks of genes encoding transcription factors and additional signals, which guide the terminal differentiation of different cell types. Most of the signalling mechanisms that establish different embryonic territories and some of the transcription factors that specify cell types are highly conserved with those that pattern vertebrate embryos. The relative simplicity of the sea urchin embryo and the existence of tools for rapidly determining gene function provide clear advantages for understanding how early developmental processes work. Key Concepts: Sea urchin embryogenesis employs the two common mechanisms of early fate specification, inheritance of maternal molecules and signalling among cells. The maternally derived initial state, in the absence of all known signals sent among the cells of the embryo, promotes development of anterior neuroectoderm, a region of ectoderm within which nerves develop. Early posterior canonical Wnt signalling activates transcription factors followed by additional signals that convert posterior blastomeres to mesoderm and endoderm and restrict the anterior neuroectoderm fate to the anterior end of the embryo. Patterning of anterior (neuroectoderm) and posterior (endomesoderm) fates requires mutual antagonism between the gene regulatory networks headed by Wnt and Six3, respectively. Nodal signalling is necessary and sufficient for specification of fates along the dorsal–ventral axis, including oral and aboral ectoderm types. Anterior–posterior (AP) and dorsal–ventral (DV) patterning are interconnected and temporally coordinated because early posterior canonical Wnt signalling is required to derepress nodal expression. The components of the major tissue territory gene regulatory networks (GRNs) have been identified by studying embryos lacking signalling through canonical Wnt, Nodal or BMP, and their functional relationships determined by knocking down each of the corresponding proteins in vivo with morpholino oligonucleotides and monitoring effects on expression of other genes. Individual cell types in sea urchin embryos are determined when their fates cannot be changed experimentally; this process requires stable activation of genes necessary for specification of a particular cell type and stable repression of those required for specification of other cell types. The GRN devices that produce stable regulatory states are reinforcing cross‐regulatory and feedback loops among the component transcription factors, which render these states insensitive to signals. The sea urchin embryo has enormous capacity before larval stages to change cell fates upon experimental challenge because the fates of many cells are only gradually specified and can be altered by signals sent from other cells.

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“…During the development, the specification of cell fate is regulated by nodal, which is responsible of the dorsal-ventral axis determination and encodes for a protein belonging to the TGF-β superfamily [49]. Modulation of nodal signalling is essential for normal patterning of D/V axis that is modulated by its antagonist, lefty.…”