Eye Development in Drosophila

果蝇tom转座因子的移动 ananassae导致自发突变的高发生率。 这些突变中的大多数显示出显性眼特异性表型， 这表明，在基因类型的高度选择性，可以是 突变的tom元件，或者可替代地，特异性， 转座因子引起突变的机制 表型初步结果表明tom-induced显性 表型是由位于邻近的基因的过度表达引起的， 到汤姆插入部位。其中一个基因叫做Om（1D）， 被分离出来，并发现编码一种含有同源框的蛋白质。 除了25种不同的光学形态（Om）突变体外， tom元素的活动允许识别 Om突变的抑制子和增强子。其中一 抑制子Om（1 K）Su逆转由以下引起的突变表型： 在所有25个Om基因中插入tom。这表明 抑制基因可以编码突变所共有的功能 在所有的Om基因座中。Corces博士假设，这种功能可能是 与TOM元件诱导过度的能力有关 突变基因的表达，以及因此Om（1 K）Su基因的表达 可以编码眼特异性转录因子， 汤姆元素。他在这里建议研究的机制， 其中TOM元件引起眼睛特异性表型， 确定受Om影响的基因在眼睛发育中的作用 突变。Om（1D）基因在组织中的特异性表达 不同的发育阶段将被确定， Om（1D）基因的隐性表型分析将是 贯彻将克隆抑制基因Om（1 K）Su， 以其表达模式为特征。它的蛋白质 用E.大肠杆菌和分离和生化分析将 用于确定这种蛋白质之间的假定相互作用 和Om（1D）基因和/或tom元件。最后 将研究TOM元件的诱变机理。 负责其致突变作用的tom元件的序列 将通过分子和遗传学的结合来识别 接近。

Mobilization of the tom transposable element in Drosophila ananassae results in high incidence of spontaneous mutations. Most of these mutations show dominant eye-specific phenotypes, suggesting a high selectivity in the type of genes that can be mutated by the tom element, or alternatively, a specificity in the mechanism by which this transposable element causes mutant phenotypes. Preliminary results suggest that tom-induced dominant phenotypes result from over-expression of genes located adjacent to the tom insertion site. One of these genes, called Om(1D), has been isolated and found to encode a homeobox containing protein. In addition to 25 different optic morphology (Om) mutants, mobilization of the tom element has allowed the identification of suppressors and enhancers of Om mutations. One of these suppressors, Om(1K)Su, reverses the mutant phenotype caused by insertion of tom in all 25 Om genes. This suggests that the suppressor gene may encode a function that is common to mutations in all Om loci. Dr. Corces hypothesizes that this function may be related to the ability of the tom element to induce over expression of the mutant gene, and therefore the Om(1K)Su gene may encode an eye specific transcription factor that interacts with the tom element. He proposes here to study the mechanisms by which the tom element causes eye specific phenotypes and determine the role in eye development of genes affected by Om mutations. The tissue specific expression of the Om(1D) gene at different developmental stages will be determined and a genetic analyses of the recessive phenotype of the Om(1D) gene will be carried out. The suppressor Om(1K)Su gene will be cloned and characterized as will its pattern of expression. Its protein will be expressed in E. coli and isolated and biochemical assays will be used to determine putative interactions between this protein and the Om(1D) gene and/or the tom element. Finally, the mechanism of mutagenesis by the tom element will be investigated. Sequences of the tom element responsible for its mutagenic effect will be identified by a combination of molecular and genetic approaches.