Integrity of the midbrain region is required to maintain the diencephalic–mesencephalic boundary in zebrafish no isthmus/pax2.1 mutants

Integrity of the midbrain region is required to maintain the diencephalic–mesencephalic boundary in zebrafish no isthmus/pax2.1 mutants
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维持斑马鱼 no isthmus/pax2.1 突变体的间脑-中脑边界需要中脑区域的完整性

DOI:
10.1002/dvdy.10384
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发表时间:
2003
影响因子:
2.5
通讯作者:
M. Brand
M. Brand
中科院分区:
生物学3区
文献类型:
--
作者:
S. Scholpp;M. Brand

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在原肠胚形成期间,神经管形成前脑、中脑和后脑原基的初始前后图案已经发生,以响应原肠胚胚胎的图案化信号。在最初建立之后,每个大脑部分的进一步发展被认为在很大程度上独立于其他部分。然而,机制应该存在,以确保适当的划分大脑的分区也在后期阶段,这样的机制,然而,知之甚少。在无峡部突变的斑马鱼胚胎中,pax 2.1基因的失活导致中脑和峡部原基从原肠胚阶段开始不能正常发育(Lun和Brand [ 1998 ] Development 125:3049-3062)。在这里,我们报告说,最初正确的建立在原肠胚阶段,邻近的前脑原基,部分,后脑原基扩展到错误指定的中脑领土没有峡部突变胚胎。这种扩张在间脑的后部尤其明显,而在第一菱形段(直接邻接中脑/峡部原基的区域)则不那么明显。后连合的核在大小上扩大,前脑和菱形节1的标记基因逐渐扩展到错误指定的中脑原基,最终导致中脑原基的重新指定。因此,我们认为Pax2.1控制的遗传程序不仅参与启动,而且还参与维持中脑和峡部细胞的身份,以防止它们承担前脑或后脑的命运。发展动力学,2003年。© 2003 Wiley利斯公司
Initial anterior–posterior patterning of the neural tube into forebrain, midbrain, and hindbrain primordia occurs already during gastrulation, in response to signals patterning the gastrula embryo. After the initial establishment, further development within each brain part is thought to proceed largely independently of the others. However, mechanisms should exist that ensure proper delineation of brain subdivisions also at later stages; such mechanisms are, however, poorly understood. In zebrafish no isthmus mutant embryos, inactivation of the pax2.1 gene leads to a failure of the midbrain and isthmus primordium to develop normally from the gastrula stage onward (Lun and Brand [ 1998 ] Development 125:3049–3062). Here, we report that, after the initially correct establishment during gastrulation stages, the neighbouring forebrain primordium and, partially, the hindbrain primordium expand into the misspecified midbrain territory in no isthmus mutant embryos. The expansion is particularly evident for the posterior part of the diencephalon and less so for the first rhombomeric segment, the territories immediately abutting the midbrain/isthmus primordium. The nucleus of the posterior commissure is expanded in size, and marker genes of the forebrain and rhombomere 1 expand progressively into the misspecified midbrain primordium, eventually resulting in respecification of the midbrain primordium. We therefore suggest that the genetic program controlled by Pax2.1 is not only involved in initiating but also in maintaining the identity of midbrain and isthmus cells to prevent them from assuming a forebrain or hindbrain fate. Developmental Dynamics, 2003. © 2003 Wiley‐Liss, Inc.
DOI: --
发表时间: 2002-08
期刊: Development
影响因子: 4.6
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DOI: --
发表时间: 2002-02
期刊: Development
影响因子: 4.6
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DOI: --
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期刊: Development
影响因子: 4.6
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发表时间: 1994-03
期刊: Development
影响因子: 4.6
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DOI: --
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期刊: Development
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