DEVELOPMENTAL PROGRAMS OF CELL CYCLE CONTROL

细胞增殖的控制对胚胎发育非常重要 和成体的组织稳定性，细胞上的约束被侵蚀 循环会导致疾病。早期胚胎细胞专门繁殖 迅速，它们这样做，排除了移动，转录和 甚至DNA紧凑成异染色质。顺序加法 细胞周期的抑制驯服了早期的猖獗的增殖 发育并为胚胎的基因表达、形态发生和 差异化。在果蝇中，S期随着转录的开始而延长， 在原肠运动时，细胞周期中增加了G2期。 开始，在细胞分化之前增加一个G1期。我们会 原样研究控制细胞周期的机制 相继转型及其对事件的影响 潜在的基因表达和形态发生。我们将在以下时间完成此工作 果蝇，它提供了一个特征良好的模型发育系统 拥有强大的遗传、分子和细胞学工具。中的更改 细胞周期调节因子的表达或降解伴随着细胞 循环过渡。例如，有丝分裂周期蛋白不断地 出现在只有S和M期的早期旋回中。他们是 在引入G2的有丝分裂时被破坏，以及它们的有丝分裂后 当引入G1时，重新积累被延迟。他们完全是 在内环中被消除。我们将调查这种自行车的多样性是如何 行为改变了周期蛋白在控制退出中的作用 有丝分裂，以及防止再次复制。探索如何协调 细胞周期与形态发生，我们将检查控制延迟 参与腹侧沟形成的细胞有丝分裂：没有这一点 延迟，有丝分裂会破坏皱纹的形成。研究细胞的作用 在基因表达周期延长的情况下，我们正在测试一种DNA 序列可以同时转录和复制，我们正在 异染色质出现的细胞周期偶联研究 这有助于基因表达的稳定失活。

The control of cell proliferation is important for embryonic development and tissue stability in the adult, where erosion of constrains on the cell cycle leads to disease. Early embryonic cell are specialized to multiply rapidly, which they do to the exclusion of movement, transcription and even the compaction of DNA into heterochromatin. The sequential addition of cell cycle constrains tames the rampant proliferation of early development and prepares the embryo for gene expression, morphogenesis and differentiation. In Drosophila, S phase lengthens as transcription begins, a G2 phase is added to the cell cycle at the time gastrulation movements begin, and a G1 phase is added prior to cellular differentiation. We will investigate the mechanisms that govern the cell cycle as it is successively transformed and the impact of these transformation on events underlying gene expression and morphogenesis. We will do this in Drosophila, which offers a well characterized model developmental system having powerful genetic, molecular and cytological tools. Changes in expression or degradation of the cell cycle regulators accompany the cell cycle transitions. For example, the mitotic cyclins are continuously present in the early cycles which have only S and M phases. They are destroyed at mitosis upon the introduction of a G2, and their post mitotic re-accumulation is delayed upon introduction of a G1. They are completely eliminated in endocycles. We will investigate how this diversity of cyclin behaviors alters the roles of the cyclins in controlling exit from mitosis, and in preventing re-replication. To explore the coordination of the cell cycle with morphogenesis, we will examine controls that delay mitosis in cells involved in ventral furrow formation: without this delay, mitosis disrupts furrow formation. To investigate the role of cell cycle lengthening in gene expression, we are testing whether a DNA sequence can be simultaneously transcribed and replicated, and we are investigating the cell cycle coupling of the appearance of heterochromatin which contributes to stable inactivation of gene expression.