DROSOPHILA MIDGUT MORPHOGENESIS REQUIRES THE FUNCTION OF THE SEGMENTATION GENE ODD-PAIRED
DROSOPHILA MIDGUT MORPHOGENESIS REQUIRES THE FUNCTION OF THE SEGMENTATION GENE ODD-PAIRED
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DOI：
10.1006/dbio.1995.1171
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发表时间：
1995-06-01
影响因子：
2.7
通讯作者：
SAKONJU, S
中科院分区：
文献类型：
--
作者：
CIMBORA, DM;SAKONJU, S
果蝇胚胎中肠的发育依赖于许多基因，包括tinman基因。和风笛，它们是内脏中胚层形成所必需的，以及同源异型基因及其靶标，它们在内脏中胚层局部作用以指导特定中肠收缩的形成。在这里，我们报告的另一个基因，奇数配对（opa），正常中肠发育所需的鉴定和表征。opa，首先通过其在幼虫角质层中的成对规则突变表型鉴定，编码含有推定的DNA结合结构域和转录调节因子的其他标志的蛋白质。我们通过将两个无效突变映射到假定的opa转录物的开放阅读框，已经将克隆的基因确定为opa;这些突变破坏开放阅读框，并产生缺乏DNA结合结构域的预测蛋白质。我们证明，opa的功能是必需的三个特征的中肠收缩的形成。为了了解opa促进缩窄形成的机制，我们分析了opa在整个中肠发育过程中的表达和功能。在细胞胚盘中，opa在外胚层和中胚层前体中普遍表达，遍及假定的分节区域。随着发育的进行，opa表达在外胚层和下面的中胚层细胞中短暂停止，这些中胚层细胞后来成为内脏中胚层。我们发现，在opa突变体的内脏中胚层被中断，显然是由于风笛，一个同源结构域基因的内脏中胚层的形成所需的异常表达。在opa突变体发育的早期阶段，沿前后轴沿着许多位置观察到内脏中胚层的中断。随着发育的进行，中断不太频繁地观察到;然而，一个中断，与apneapedia表达域一致，总是持续存在。这种持续性缺陷显然是导致opa突变体中触角足表达丧失和超双胸表达变异的原因。从这些观察结果，我们推断，在opa突变体中至少第一和第二中肠收缩的损失是在内脏中胚层发育的早期阶段首先明显的缺陷的结果。在发育的后期阶段，opa的表达在内脏中胚层的空间限制区域重新启动，与第一和第三缩窄形成的位置一致。opa表达的这些结构域是由同源异型基因和分泌的生长因子调节的结果，所述同源异型基因和分泌的生长因子局部作用以指导缢痕形成。在第一和第三紧缩的位置，opa是正调控的adminapedia和abdominal-A，分别，而这些域之间的opa是负调控的Ultrabithorax和decapentaplegic。opa的巧合。在第一和第三中肠缩窄部的位置的表达以及已知指导缩窄部形成的基因对OPA表达的复杂调节使我们推测，除了有助于内脏中胚层发育之外，OPA还可能在中肠缩窄部形成期间介导同源异型基因功能。(C)出版社：Academic Press
Development of the Drosophila embryonic midgut is dependent on a number of genes, including tinman. and bagpipe, which are required for formation of the visceral mesoderm, and the homeotic genes and their targets, which act locally in the visceral mesoderm to direct formation of specific midgut constrictions. Here we report the identification and characterization of another gene, odd-paired (opa), required for normal midgut development. opa, first identified by its pair-rule mutant phenotype in the larval cuticle, encodes a protein containing putative DNA binding domains and other hallmarks of transcriptional regulators. We have positively identified the cloned gene as opa by mapping two null mutations to the open reading frame of the putative opa transcript; these mutations disrupt the open reading frame and generate predicted proteins lacking the DNA binding domain. We demonstrate that opa function is required for formation of the three characteristic midgut constrictions. To understand the mechanisms by which opa contributes to constriction formation, we have analyzed the expression and function of opa throughout midgut development. In the cellular blastoderm, opa is expressed ubiquitously in the ectoderm and mesoderm precursors throughout the presumptive segmented region. As development proceeds, opa expression ceases briefly both in the ectoderm and in the underlying mesodermal cells that later become the visceral mesoderm. We show that in opa mutants the visceral mesoderm is interrupted, evidently due to abnormal expression of bagpipe, a homeodomain gene required for the formation of the visceral mesoderm. At early stages of development in opa mutants, interruptions in the visceral mesoderm are observed at many positions along the anterior-posterior axis. As development proceeds, interruptions are less frequently observed; however, one interruption, coincident with the Antennapedia expression domain, invariably persists. This persistent defect is apparently responsible for the loss of Antennapedia expression and variability of Ultrabithorax expression in opa mutants. From these observations, we infer that the loss of at least the first and second midgut constrictions in opa mutants is the result of defects first evident in the early stages of visceral mesoderm development. During later stages in development, opa expression reinitiates in spatially restricted domains of the visceral mesoderm, coinciding with the locations at which the first and third constrictions will form. These domains of opa expression are the result of regulation by the homeotic genes and a secreted growth factor, which act locally to direct constriction formation. At the locations of the first and third constrictions, opa is positively regulated by Antennapedia and abdominal-A, respectively, while between these domains opa is negatively regulated by Ultrabithorax and decapentaplegic. The coincidence of opa. expression with the locations of the first and third midgut constrictions and the complex regulation of opa expression by genes known to direct constriction formation lead us to speculate that in addition to contributing to visceral mesoderm development, opa may mediate homeotic gene function during midgut constriction formation. (C) 1995 Academic Press,Inc.