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Axial level‐dependent molecular and cellular mechanisms underlying the genesis of the embryonic neural plate
Author(s) -
Kondoh Hisato,
Takada Shinji,
Takemoto Tatsuya
Publication year - 2016
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1111/dgd.12295
Subject(s) - neural plate , enhancer , epiblast , neural tube , sox2 , paraxial mesoderm , biology , microbiology and biotechnology , embryonic stem cell , mesoderm , neurulation , transcription factor , anatomy , genetics , embryogenesis , gastrulation , embryo , gene
The transcription factor gene Sox2 , centrally involved in neural primordial regulation, is activated by many enhancers. During the early stages of embryonic development, Sox2 is regulated by the enhancers N2 and N1 in the anterior neural plate ( ANP ) and posterior neural plate ( PNP ), respectively. This differential use of the enhancers reflects distinct regulatory mechanisms underlying the genesis of ANP and PNP . The ANP develops directly from the epiblast, triggered by nodal signal inhibition, and via the combined action of TF s SOX 2, OTX 2, POU 3F1, and ZIC 2, which promotes the the ANP development and inhibits other cell lineages. In contrast, the PNP is derived from neuromesodermal bipotential axial stem cells that develop into the neural plate when Sox2 is activated by the N1 enhancer, whereas they develop into the paraxial mesoderm when the N1 enhancer is repressed by the action of TBX 6. The axial stem cells are maintained by the activity of WNT 3a and T (Brachyury). However, at axial levels more anterior to the 8th somites (cervical levels), the development of both the neural plate and somite proceeds in the absence of WNT 3a, T, or TBX 6. These observations indicate that distinct molecular and cellular mechanisms determine neural plate genesis based on the axial level, and contradict the classical concept of the term “neural induction,” which assumes a pan‐neural plate mechanism.