Abstract
When early canonical Wnt is experimentally inhibited, sea urchin embryos embody the concept of a Default Model in vivo because most of the ectodermal cell fates are specified as anterior neuroectoderm. Using this model, we describe here how the combination of orthogonally functioning anteroposterior Wnt and dorsoventral Nodal signals and their targeting transcription factors, FoxQ2 and Homeobrain, regulates the precise patterning of normal neuroectoderm, of which serotonergic neurons are differentiated only at the dorsal/lateral edge. Loss-of-function experiments revealed that ventral Nodal is required for suppressing the serotonergic neural fate in the ventral side of the neuroectoderm through the maintenance of foxQ2 and the repression of homeobrain expression. In addition, non-canonical Wnt suppressed homeobrain in the anterior end of the neuroectoderm, where serotonergic neurons are not differentiated. Canonical Wnt, however, suppresses foxQ2 to promote neural differentiation. Therefore, the three-dimensionally complex patterning of the neuroectoderm is created by cooperative signals, which are essential for the formation of primary and secondary body axes during embryogenesis.
Highlights
Embryonic cells of some animals tend to be differentiated into neuroectoderm cells/neural progenitors unless they receive an extrinsic signal, so-called default model [1,2]
The sea urchin embryo is similar to vertebrate embryos in that the default cell fate is potentially neurogenic, and normal development restricts the neural fate to the narrow area that locates at the anterior/dorsal region of the embryo
We describe how the combination of orthogonally functioning signaling pathways regulates their targeting transcription factors expressing at the anterior neuroectoderm to restrict and pattern the default neurogenic region
Summary
Embryonic cells of some animals tend to be differentiated into neuroectoderm cells/neural progenitors unless they receive an extrinsic signal, so-called default model [1,2]. Chordin and Noggin, which were initially reported as neural inducers, function in protecting the initial neuroectodermal fate at the dorsal side in vertebrates from invading bone morphogenetic protein (BMP) signals that are expressed at the ventral side and that specify a non-neuroectodermal fate [2] Wnts, another type of secreted signaling molecule, have functions in repressing the initial anterior neuroectodermal fate. Posteriorly functioning Wnt inhibits anterior neuroectoderm specification genes, such as otx, and leads to the specification of posterior neuroectoderm [5] Together, these secreted signaling molecules that regulate body axis formation act to suppress the initial neuroectodermal fate during early embryogenesis. Within the remaining initial neurogenic ectoderm, each terminal cell differentiation is precisely controlled to organize the complicated neural network, i.e., the patterning of the neurogenic ectoderm is highly sophisticated in the restricted neuroectoderm of normal embryos
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