Direct development of neurons within foregut endoderm of sea urchin embryos
Direct development of neurons within foregut endoderm of sea urchin embryos
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DOI：
10.1073/pnas.1018513108
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发表时间：
2011-05-31
影响因子：
11.1
通讯作者：
Angerer, Lynne M.
中科院分区：
文献类型：
--
作者：
Wei, Zheng;Angerer, Robert C.;Angerer, Lynne M.
虽然它是公认的，神经细胞是外胚层衍生物在bilaterian动物，在这里，我们报告了令人惊讶的发现，一些海胆胚胎的咽神经元从头发展的内胚层。这些神经元的外观是独立的口的形成，其中口的外胚层加入前肠。神经元并不来源于外胚层细胞迁移到前肠，如用光活化蛋白KikGR的谱系追踪所示。它们的特化和发育取决于Nkx 3 -2的表达，Nkx 3 -2又取决于Six 3，两者都在前肠谱系中表达。SoxB 1，这是密切相关的脊椎动物的Sox因子，支持神经前体状态，也表达在整个原肠胚形成的前肠，这表明该地区的完全形成的原肠保留了意想不到的多能性。总之，这些结果导致了意想不到的结论，即在已经被完善的基因调控网络指定为内胚层的细胞谱系内[Peter IS，Davidson EH（2010）Dev Biol 340：188-199]，还运行着咽部中的一些神经元的从头指定所需的Six 3/Nkx 3 -2依赖性途径。因此，神经内胚层前体在前肠中形成，这有助于保持SoxB 1依赖性多能状态。
Although it is well established that neural cells are ectodermal derivatives in bilaterian animals, here we report the surprising discovery that some of the pharyngeal neurons of sea urchin embryos develop de novo from the endoderm. The appearance of these neurons is independent of mouth formation, in which the stomodeal ectoderm joins the foregut. The neurons do not derive from migration of ectoderm cells to the foregut, as shown by lineage tracing with the photoactivatable protein KikGR. Their specification and development depend on expression of Nkx3-2, which in turn depends on Six3, both of which are expressed in the foregut lineage. SoxB1, which is closely related to the vertebrate Sox factors that support a neural precursor state, is also expressed in the foregut throughout gastrulation, suggesting that this region of the fully formed archenteron retains an unexpected pluripotency. Together, these results lead to the unexpected conclusion that, within a cell lineage already specified to be endoderm by a well-established gene regulatory network [Peter IS, Davidson EH (2010) Dev Biol 340: 188-199], there also operates a Six3/Nkx3-2-dependent pathway required for the de novo specification of some of the neurons in the pharynx. As a result, neuroendoderm precursors form in the foregut aided by retention of a SoxB1-dependent pluripotent state.