ANALYSIS OF PRIMARY PALATE FORMATION

对初级腭发育机制的理解 需要在与以下方面有关的研究方面取得进一步进展： 唇腭裂等畸形。 根据我们过去的研究， 确定了一个有序的，连续的细胞死亡率下降模式， 扩散造成了地区性的增长率差异 在鸟类胚胎的主要上颚 的这种模式 下降与亚群的出现密切相关， 从快速增殖池中退出的细胞， 安静。 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被发现，这些细胞经历 在明显的软骨形成之前的细胞周期阻滞。 相关研究 细胞通讯显示，缝隙连接的分布是 非随机的，最高浓度是在 上颌突的上皮下间质。 这些数据，当 与我们相同区域的细胞周期数据相结合，表明 细胞通信模式之间存在关系， 细胞周期动力学和上皮-间质相互作用的变化。 未来的工作将致力于确定（1）在多大程度上 上皮-间充质相互作用对于诱导或 维持细胞通信模式，（2）是否 上皮-间充质相互作用对于维持细胞增殖是必要的。 （3）增殖率的先后顺序， 潜在的因果关系，存在之间的变化， 上皮-间质相互作用，细胞形态改变， 通信和维持细胞增殖速率，以及（4） 确定细胞通讯解偶联对细胞周期的影响 进展 荧光免疫细胞化学，透射电镜 显微镜、放射自显影、器官培养和组织重组 将采用技术。 显微注射单个细胞， 27，000道尔顿间隙连接蛋白的抗体将用于阻断 细胞通讯 该项目的研究结果将在 其他研究，以分析畸形的发病机制， 哺乳动物胚胎

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.