Embryonic Salivary Gland Development in Drosophila

描述：拟议研究是申请人广泛兴趣的一部分， 建立不同组织和器官的遗传机制， 胚胎发生，包括定义器官的初始指令和 随后的细胞-细胞信号传导、基因表达的变化和细胞 这些运动建立了分化的器官并保持了它的身份。研究 果蝇胚胎中唾液腺发育的研究， 唾液原基中细胞的初步测定。唾液基因 表达被同源异型基因性梳减少激活， 唾液腺和唾液腺导管原基彼此的区别在于： EGF受体信号通路的相反活性和 转录因子叉头。然而，无论是效应器还是 EGFR信号传导的靶点已经确定。在他们做出决定后不久， 唾液腺开始形成的有序内陷，开始于 基板的后背侧边缘，并继续到前面，然后 基板的腹侧部分。导管由基板的延续形成 内陷产生直径小得多的Y形导管 而不是腺体。虽然这种形态发生是高度有序的，但其遗传 控制才刚刚开始研究。有五个具体目标， 这些实验：1）鉴定阻止FKH的Spitz依赖性阻遏物 在导管前细胞中表达。2)定义无意义的角色， 没有女儿它们是否拮抗EGFR通路的作用; 3）确定 huckebein和wingless是否相互作用以启动和组织唾液 内陷; 4）测试Tec 29酪氨酸激酶是否调节细胞分裂 在唾液基板，以促进唾液形态发生;和5）使用 致敏遗传筛选以鉴定唾液管所需的基因 发展

DESCRIPTION: The proposed study is part of a broad interest by the applicant in the genetic mechanisms that establish distinct tissues and organs during embryogenesis, including both the initial instructions that define an organ and the subsequent cell-cell signaling, changes in gene expression, and cellular movements that build the differentiated organ and maintain its identity. Study of salivary gland development in Drosophila embryos has led to a model for the initial determination of cells in the salivary primordium. Salivary gene expression is activated by the homeotic gene Sex combs reduced, and the salivary gland and salivary duct primordia are distinguished from each other by the opposing activities of the EGF receptor signaling pathway and the transcription factor fork head. Nevertheless, neither the effectors nor the targets of EGFR signaling have been defined. Shortly after their determination, salivary glands begin to form by an orderly invagination that begins at the posterior dorsal edge of the placode and continues to the anterior and then ventral parts of the placode. The ducts form by a continuation of the placode invagination to produce the Y-shaped ducts that are much smaller in diameter than the glands. Although this morphogenesis is highly ordered, its genetic control is just beginning to be investigated. There are five Specific Aims for these experiments: 1) identify the spitz-dependent repressors that prevent fkh expression in the pre-duct cells. 2) define the roles of senseless and daughterless. Do they antagonize the effects of the EGFR pathway; 3) determine whether huckebein and wingless interact to initiate and organize salivary invagination; 4) test whether the Tec29 tyrosine kinase regulates cell division in the salivary placode to facilitate salivary morphogenesis; and 5) use a sensitized genetic screen to identify genes required for salivary duct development.