ANALYSIS OF PRIMARY PALATE FORMATION

对初级腭部发育的机制的理解 是取得进一步进展所必需的，这与 唇腭裂等畸形。从我们过去的研究来看，我们有 确定了细胞速率的有序、连续的下降模式 扩散造成地区特定增长率的差异 遍及鸟类胚胎的主要味觉。这种模式 下降与亚群的出现密切相关。 从快速增殖的池中出来的细胞，似乎是 一动不动。最近的研究表明，静止和/或缓慢循环的细胞 最终在软骨形成区域发现，这些细胞经历了 在明显的软骨形成之前，细胞周期受阻。相关的研究成果 细胞通讯显示，缝隙连接的分布是 非随机的，浓度最高的是 上颌突上皮下间质。这些数据，当 结合我们在相同地区的细胞周期数据，表明 细胞通讯的模式之间存在着关系，细胞通讯的模式 细胞周期动力学的改变，以及上皮-间充质的相互作用。 未来的努力将指向确定(1)在多大程度上 上皮-间充质相互作用是诱导血管内皮细胞分化所必需的 信元通信模式的维持，(2)是否 上皮-间充质相互作用是细胞维持所必需的 在下层间充质中的增殖率，(3)什么顺序，以及 潜在的因果关系，存在于 上皮-间充质相互作用，细胞形态的变化 通信和维持细胞增殖率，以及(4) 确定细胞通讯解偶联对细胞周期的影响 进步。荧光免疫细胞化学、透射电子 显微镜、放射自显影、器官培养和组织重组 将采用各种技术。单个细胞的显微注射 27000道尔顿缝隙连接蛋白的抗体将被用来阻断 蜂窝通讯。该项目的研究结果将在 其他分析儿童畸形发病机制的研究 哺乳动物的胚胎。

An understanding of the mechanisms that underlie primary palate development is necessary for further progress to be made in research related to malformations such as cleft lip and palate. From our past studies we have determined that an orderly, sequential pattern of decline in rates of cell proliferation produces region-specific differences in growth rates throughout the primarly palate of the avian embryo. This pattern of decline was closely associated with the appearance of subpopulations of cells which exit from rapidly proliferating pools and which appeared to be quiescent. Recent studies suggest that quiescent and/or slow cycling cells were ultimately found in chondrogenic regions and that these cells undergo a cell cycle block prior to overt chondrogenesis. Correlative studies of cell communication revealed that the distribution of gap junctions was non-random and that the highest concentrations were found in the subepithelial mesenchyme of the maxillary process. These data, when integrated with our cell cycle data for the same regions, suggest that relationships exist between patterns of cell communication, the pattern of change in cell cycle kinetics, and epithelial-mesenchymal interaction. Future efforts will be directed toward determining (1) the extent to which epithelial-mesenchymal interaction is necessary for the induction or maintenance of patterns of cell communication, (2) whether epithelial-mesenchymal interaction is necessary for the maintenance of cell proliferation rates in subjacent mesenchyme, (3) what sequential, and potentially causal, relationships exist between alterations in epithelial-mesenchymal interaction, changes in the pattern of cell communication and the maintenance of cell proliferation rates, and (4) to determine the effect of uncoupling of cell communication on cell cycle progression. Fluorescence immunocytochemistry, transmission electron microscopy, autoradiography, organ culture, and tissue recombination techniques will be employed. Microinjection of individual cells with antibody to the 27,000 dalton gap junctional protein will be used to block cell communication. The findings from this project will be extended in other studies for analysis of the pathogenesis of malformations in mammalian embryos.