Peanut agglutinin and chondroitin-6-sulfate are molecular markers for tissues that act as barriers to axon advance in the avian embryo.
Peanut agglutinin and chondroitin-6-sulfate are molecular markers for tissues that act as barriers to axon advance in the avian embryo.
复制标题
花生凝集素和 6-硫酸软骨素是组织的分子标记，在禽类胚胎中充当轴突前进的障碍。
DOI：
10.1016/s0012-1606(05)80017-x
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发表时间：
1991
影响因子：
2.7
通讯作者：
Tosney,KW
中科院分区：
文献类型：
--
作者：
Oakley,RA;Tosney,KW
鸡胚脊髓和后肢之间轴突的生长受到轴突通路边界的三种组织的限制。生长锥转向，以避免在正常发育过程中和实验操作后的后硬骨节，perinotochordal间充质，和骨盆带前体。我们想知道这些功能相似的轴突前进障碍是否也有共同的分子组成。由于后硬化体差异结合花生凝集素（PNA），因为PNA结合也是典型的前软骨分化，我们研究了PNA结合位点和软骨蛋白多糖表位的表达模式与轴突生长。我们发现，所有三个屏障组织优先表达PNA结合位点和软骨素-6-硫酸（C-6-S）的免疫反应性的时候，生长锥避免这些组织。此外，这两个表位在脊髓的顶板和早期肢芽中表达，这是轴突前进的两个额外的假定障碍。相比之下，在外周轴突通路中均未检测到表位。在体节中，这种二分法的表达模式明显先于运动生长锥或神经嵴细胞对前硬节的入侵。然而，在肢体中，屏障标记物从假定的轴突通路中消失，与轴突的入侵一致。由于这种坐标模式表明，在这些轴突通路的屏障标记物的情况下，需要与生长锥的相互作用，我们分析了屏障标记物的表达模式后，单侧神经管缺失。我们发现，PNA阴性轴突通路正常发展，即使在虚拟的轴突生长的情况下。我们的结论是，没有染色与碳水化合物特异性屏障标记物是一个独立的特征，包括轴突通路的细胞。这些结果确定了两个分子标记物，其特征在于已知的功能障碍轴突前进，并建议屏障组织可能会强加模式外周神经生长凭借其独特的分子组成。
Axon outgrowth between the spinal cord and the hindlimb of the chick embryo is constrained by three tissues that border axon pathways. Growth cones turn to avoid the posterior sclerotome, perinotochordal mesenchyme, and pelvic girdle precursor during normal development and after experimental manipulation. We wanted to know if these functionally similar barriers to axon advance also share a common molecular composition. Since the posterior sclerotome differentially binds peanut agglutinin (PNA) and since PNA binding is also typical of prechondrogenic differentiation, we examined the pattern of expression of PNA binding sites and cartilage proteoglycan epitopes in relation to axon outgrowth. We found that all three barrier tissues preferentially express both PNA binding sites and chondroitin-6-sulfate (C-6-S) immunoreactivity at the time when growth cones avoid these tissues. Moreover, both epitopes are expressed in the roof plate of the spinal cord and in the early limb bud, two additional putative barriers to axon advance. In contrast, neither epitope is detected in peripheral axon pathways. In the somites, this dichotomous pattern of expression clearly preceded the invasion of the anterior sclerotome by either motor growth cones or neural crest cells. However, in the limb, barrier markers disappeared from presumptive axon pathways in concert with the invasion of axons. Since this coordinate pattern suggested that the absence of barrier markers in these axon pathways requires an interaction with growth cones, we analyzed the pattern of barrier marker expression following unilateral neural tube deletions. We found that PNA-negative axon pathways developed normally even in the virtual absence of axon outgrowth. We conclude that the absence of staining with carbohydrate-specific barrier markers is an independent characteristic of the cells that comprise axon pathways. These results identify two molecular markers that characterize known functional barriers to axon advance and suggest that barrier tissues may impose patterns on peripheral nerve outgrowth by virtue of their distinct molecular composition.