DROSOPHILA PATTERN REPAIR--GENETIC AND CELLULAR ANALYSIS

模式的建立是发育生物学的一个重要课题， 无论是在分子、细胞还是解剖学水平上进行研究。 虽然大量的重点放在应用的工具， 分子生物学和遗传学对模式出现的研究， 初步研究了模具的维护与修理问题 从解剖学的角度来看。肢体再生（英语：limb regeneration） 昆虫和两栖动物）和成虫盘修复（昆虫）是例子 模式修复。我们提出胚胎模式修复的存在 系统（Prs）基因负责检测和修复 果蝇胚胎发育过程中的模式错误。我们有 开始分离和分析影响胚胎模式的突变 修复. 在实验中观察到胚胎模式修复， 调节母体效应基因Bicoid（BCD）。在卵子发生过程中， bcd mRNA锚定在卵母细胞的前端。bcd翻译 施肥后的信息导致BCD的浓度梯度 蛋白质，这反过来又触发了一系列转录事件， 导致前部结构的规格（重复 在没有BCD活性的情况下观察到后部结构）。 减少或增加bcd基因剂量从一个到四个拷贝，两个 拷贝数是正常的补体，引起前形态学上的一些改变。 标记分别向前或向后移动。人会 预计相应的大小减少或增加幼虫前 结构或可能降低生存能力。出乎意料的是，两人 这些胚胎类型发育产生具有生存能力的"正常"幼虫， 生育力与野生型相同。这些观察结果表明，胚胎 具有补偿由以下因素引起的模式扰动的能力 BCD梯度的变化。正是这种补偿反应， 归因于模式修复系统。 模式修复何时以及如何发生？为了理解 胚胎对模式缺陷的反应，必须有一个详细的命运图， 包括细胞迁移信息的受影响区域， 形状有丝分裂和死亡我们已经开发出了有选择地标记 活胚胎中的单个细胞， 发展此外，我们和其他人已经制定了协议， 监测活胚胎中的细胞死亡。如此详细的命运地图， 野生型胚胎，我们将能够确定细胞的变化， 模式修复过程中的行为。 哪些基因参与了模式修复？模式修复基因将 通过观察胚胎被放置在 具有六个bcd基因拷贝的女性的生存能力降低。因此，我们认为， 在四到六个拷贝之间存在模式修复的阈值， bcd基因一种基因筛选显性突变， 具有四个bcd基因拷贝的雌性产下的胚胎的生存能力 已经启动并将延长。prs突变将在 分子和细胞水平。

Establishment of pattern is a major theme in developmental biology, whether it is studied at the molecular, cellular, or anatomical level. While a great deal of emphasis has been placed on applying the tools of molecular biology and genetics to the study of pattern emergence, the problem of maintenance and repair of pattern has been studied primarily from an anatomical viewpoint. Processes such as limb regeneration (in insects and amphibians) and imaginal disk repair (in insects) are examples of pattern repair. We propose the existence of embryonic Pattern repair system (Prs) genes that are responsible for the detection and the repair of pattern errors during Drosophila melanogaster embryogenesis. We have begun isolating and analyzing mutations that effect embryonic pattern repair. Embryonic pattern repair is observed in experiments where the dosage of the maternal effect gene, bicoid (bcd), is modulated. During oogenesis, bcd mRNA is anchored at the anterior end of the oocyte. Translation of bcd message upon fertilization results in a concentration gradient of BCD protein, which in turn triggers a cascade of transcriptional events that result in the specification of anterior structures (duplication of posterior structures is observed in the absence of BCD activity). Decreasing or increasing the bcd gene dosage from one to four copies, two copies is the normal complement, causes a number of anterior morphological markers to be shifted anteriorly or posteriorly, respectively. One would expect a corresponding size decrease or increase in larval anterior structures or possibly a reduction of viability. Unexpectedly, both of these embryo types develop to produce 'normal' larvae with viability and fertility equal to wild-type. These observations indicate that the embryo has the capacity to compensate for the pattern perturbations caused by changes in the BCD gradient. It is this compensatory response we are attributing to the pattern repair system. When and how does the pattern repair occur? In order to understand how the embryo responds to a pattern defect, one must have a detailed fate map of the affected area that includes information about cellular migration, shape, mitosis, and death. We have developed tools for selectively marking individual cells in live embryos and following their behavior through development. In addition, we and others have developed protocols for monitoring cell death in live embryos. With such a detailed fate map for wild-type embryos, we will be able to determine the changes in cellular behavior during the pattern repair process. What are the genes involved in pattern repair? Pattern repair genes will be identified by taking advantage of the observation that embryos laid by females with six copies of the bcd gene have reduced viability. Therefore, there is a threshold for pattern repair between four and six copies of the bcd gene. A genetic screen for dominant mutations that decrease the viability of embryos that laid by females with four copies of the bcd gene has been initiated and will be extended. Prs mutations will be analyzed at the molecular and cellular levels.