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Mechanisms of Translocation of and Gene Regulation by Transposable Elements in Eukaryotes

真核生物中转座元件的易位和基因调控机制

基本信息

批准号：
62480466
负责人：
SAIGO Kaoru
金额：
$ 4.16万
依托单位：
The University of Tokyo (1988)Kyushu University (1987)
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

In the present work, the following two lines of experiments were carried out and the abnormal optic morphologies in Bar and Om(1D) mutants of Drosophila were shown to be resulted from the insertional activation of a new, common homeobox-containing gene, Om(1D)/bar gene.EXP.1:The tom element, putatively associated with optic morphology mutations in Drosophila ananassae was identified as a retrovirus-like transposoble element. The tom element was found to terminate with 475 base pair direct repeats which are identical in sequence to each other. Southern blot and heteroduplex analyses showed the tom element to have high homology to 297 and 17.6, two retrotransposons found in D.melanogaster. As in the cases of 297 and 17.6, tom includes the nucleotide seqeuences coding for a presumptive protease and reverse transcriptase, similar in amino acid sequence to those of the Moloney murine leukaemia virus. The insertion of tom appears to be carried out in a sequence specific fashion using ATAT as a target.EXP.2:The genome structures of various Om(1D) alleles together with their revertants were analyzed and it was found that the activation of a newly identified, homeobox-containing Om(1D) gene by the inserted tom element to be the primary cause of Om(1D) mutations. Cytological experiments show the D.melanogaster Om(1D) gene to be located near the bar locus and duplicated in the Bar mutant. The predicted Om(1D) proteins in D.ananassae and D.melanogaster, respectively, are 603 and 542 amino acids long. Taken together, our results suggest that the Om(1D) protein may be involved in the processes for size and shape detremination of the complex eyes.

在本研究中，我们进行了以下两项实验，发现果蝇的Bar和Om（1D）突变体的光学形态异常是由一个新的、常见的同源盒基因Om(1D)/ Bar基因exp的插入激活引起的。1：被认为与果蝇的光学形态突变有关的tom元件被鉴定为逆转录病毒样转座元件。发现tom元件终止于475个碱基对直接重复序列，这些重复序列彼此相同。Southern blot和异双工分析表明，tom元件与d.m anogaster的两个反转录转座子297和17.6具有高度的同源性。与297和17.6的病例一样，tom包含了推定为蛋白酶和逆转录酶的核苷酸序列，与Moloney小鼠白血病病毒的氨基酸序列相似。tom的插入似乎是使用ATAT作为target.EXP以序列特定的方式执行的。2 .分析了Om（1D）等位基因的基因组结构及其返回物，发现插入的tom元件激活了一个新发现的含有同源盒的Om（1D）基因是Om（1D）突变的主要原因。细胞学实验表明，d.m anogaster Om（1D）基因位于bar位点附近，并在bar突变体中复制。预测的D.ananassae和D.melanogaster的Om（1D）蛋白长度分别为603和542个氨基酸。综上所述，我们的研究结果表明，Om（1D）蛋白可能参与了复杂眼睛的大小和形状决定过程。