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Tfap2 and Sox1/2/3 cooperatively specify ectodermal fates in ascidian embryos
Author(s) -
Kaoru S. Imai,
Hiroki Hikawa,
Kenji Kobayashi,
Yutaka Satou
Publication year - 2016
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.142109
Subject(s) - biology , ectoderm , embryo , cell fate determination , microbiology and biotechnology , fibroblast growth factor , neural development , fate mapping , fgf and mesoderm formation , developmental biology , genetics , anatomy , embryogenesis , stem cell , gene , transcription factor , receptor , progenitor cell
Epidermis and neural tissues differentiate from the ectoderm in animal embryos. Although epidermal fate is thought to be induced in vertebrate embryos, embryological evidence has indicated that no intercellular interactions during early stages are required for epidermal fate in ascidian embryos. To test this hypothesis, we determined the gene regulatory circuits for epidermal and neural specification in the ascidian embryo. These circuits started with Tfap2-r.b and Sox1/2/3, which are expressed in the ectodermal lineage immediately after zygotic genome activation. Tfap2-r.b expression was diminished in the neural lineages upon activation of fibroblast growth factor signaling, which is known to induce neural fate, and sustained only in the epidermal lineage. Tfap2-r.b specified the epidermal fate cooperatively with Dlx.b, which was activated by Sox1/2/3 This Sox1/2/3-Dlx.b circuit was also required for specification of the anterior neural fate. In the posterior neural lineage, Sox1/2/3 activated Nodal, which is required for specification of the posterior neural fate. Our findings support the hypothesis that the epidermal fate is specified autonomously in ascidian embryos.

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