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Pax-3的表达是由组织者和后轴旁中胚层产生的后化信号在早期神经板中启动的。

Expression of Pax-3 is initiated in the early neural plate by posteriorizing signals produced by the organizer and by posterior non-axial mesoderm.

作者信息

Bang A G, Papalopulu N, Kintner C, Goulding M D

机构信息

Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

出版信息

Development. 1997 May;124(10):2075-85. doi: 10.1242/dev.124.10.2075.

Abstract

Pax-3 is a paired-type homeobox gene that is specifically expressed in the dorsal and posterior neural tube. We have investigated inductive interactions that initiate Pax-3 transcript expression in the early neural plate. We present several lines of evidence that support a model where Pax-3 expression is initiated by signals that posteriorize the neuraxis, and then secondarily restricted dorsally in response to dorsal-ventral patterning signals. First, in chick and Xenopus gastrulae the onset of Pax-3 expression occurs in regions fated to become posterior CNS. Second, Hensen's node and posterior non-axial mesoderm which underlies the neural plate induce Pax-3 expression when combined with presumptive anterior neural plate explants. In contrast, presumptive anterior neural plate explants are not competent to express Pax-3 in response to dorsalizing signals from epidermal-ectoderm. Third, in a heterospecies explant recombinant assay with Xenopus animal caps (ectoderm) as a responding tissue, late, but not early, Hensen's node induces Pax-3 expression. Chick posterior non-axial mesoderm also induces Pax-3, provided that the animal caps are neuralized by treatment with noggin. Finally we show that the putative posteriorizing factors, retinoic acid and bFGF, induce Pax-3 in neuralized animal caps. However, blocking experiments with a dominant-inhibitory FGF receptor and a dominant-inhibitory retinoic acid receptor suggest that Pax-3 inductive activities arising from Hensen's node and posterior non-axial mesoderm do not strictly depend on FGF or retinoic acid.

摘要

Pax-3是一种配对型同源框基因,在背侧和后神经管中特异性表达。我们研究了在早期神经板中启动Pax-3转录本表达的诱导性相互作用。我们提供了几条证据支持这样一个模型:Pax-3的表达由使神经轴后化的信号启动,然后响应背腹模式信号在背侧进行二次限制。首先,在鸡和非洲爪蟾原肠胚中,Pax-3表达的起始发生在注定要形成后中枢神经系统的区域。其次,亨氏结和位于神经板下方的后非轴中胚层与假定的前神经板外植体结合时可诱导Pax-3表达。相比之下,假定的前神经板外植体不能响应来自表皮外胚层的背化信号而表达Pax-3。第三,在以非洲爪蟾动物帽(外胚层)作为反应组织的异种外植体重组试验中,晚期而非早期的亨氏结可诱导Pax-3表达。鸡的后非轴中胚层也可诱导Pax-3,前提是动物帽经诺金处理而神经化。最后我们表明,假定的后化因子视黄酸和碱性成纤维细胞生长因子(bFGF)可在神经化的动物帽中诱导Pax-3。然而,用显性抑制性成纤维细胞生长因子受体和显性抑制性视黄酸受体进行的阻断实验表明,亨氏结和后非轴中胚层产生的Pax-3诱导活性并不严格依赖于成纤维细胞生长因子或视黄酸。

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