Foxg1 confines Cajal-Retzius neuronogenesis and hippocampal morphogenesis to the dorsomedial pallium
Foxg1 confines Cajal-Retzius neuronogenesis and hippocampal morphogenesis to the dorsomedial pallium
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DOI：
10.1523/jneurosci.4804-04.2005
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发表时间：
2005-04-27
影响因子：
5.3
通讯作者：
Mallamaci, A
中科院分区：
文献类型：
--
作者：
Muzio, L;Mallamaci, A
有人建议，大脑皮层区域化依赖于位置值赋予早期皮层神经母细胞的转录因子基因内表达的苍白球领域的分级方式。Foxg 1，编码这些因素之一，以前被报道是必要的基底神经节形态发生，适当调整皮质神经元分化率，和切换的皮质神经母细胞从早期一代的原始丛状层到后期生产的皮质板。此外，Foxg 1表达呈沿着从头侧/外侧（高）到尾侧/内侧（低）的梯度，可能作为尾内侧命运的抑制因子，有助于形成皮质区域轮廓。我们用各种方法检验了这一预测，发现它是正确的。我们发现，Cajal-Retzius神经元的过度生产特征Foxg 1（-/-）突变体并不产生具体的新皮层神经母细胞的层状组织发生进展的阻塞，如前所述，而是反映了从外侧到内侧的皮质原基的再图案化。即使缺乏新皮质板，Foxg 1（-/-）胚胎也会产生结构，这些结构在分子特性和出生日期方面非常类似于海马板和齿状叶片。值得注意的是，在没有Foxg 1的情况下，额外的中间命运启动子Emx 2的失活，虽然不抑制皮质特化，但相反地挽救了神经元上的Reelin的过度产生。
It has been suggested that cerebral cortex arealization relies on positional values imparted to early cortical neuroblasts by transcription factor genes expressed within the pallial field in graded ways. Foxg1, encoding for one of these factors, previously was reported to be necessary for basal ganglia morphogenesis, proper tuning of cortical neuronal differentiation rates, and the switching of cortical neuroblasts from early generation of primordial plexiform layer to late production of cortical plate. Being expressed along a rostral/lateral(high)-to-caudal/ medial(low) gradient, Foxg1, moreover, could contribute to shaping the cortical areal profile as a repressor of caudomedial fates. We tested this prediction by a variety of approaches and found that it was correct. We found that overproduction of Cajal - Retzius neurons characterizing Foxg1(-/-) mutants does not arise specifically from blockage of laminar histogenetic progression of neocortical neuroblasts, as reported previously, but rather reflects lateral-to-medial repatterning of their cortical primordium. Even if lacking a neocortical plate, Foxg1(-/-) embryos give rise to structures, which, for molecular properties and birthdating profile, are highly reminiscent of hippocampal plate and dentate blade. Remarkably, in the absence of Foxg1, additional inactivation of the medial fates promoter Emx2, although not suppressing cortical specification, conversely rescues overproduction of Reelin on neurons.