Poster
# 16
Poster |
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6th Internet World Congress for Biomedical Sciences |
Monica Acosta(1), Kiyohito Yoshida(2)
(1)(2)Hokkaido University - Sapporo. Japan
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[Cell Biology & Cytology] |
[Genetics & Bioinformatics] |
Drosophila ananassae is a member of the melanogaster species group. In 1984, Dr. Claude W. Hinton discovered and genetically characterized a serie of mutations in D. ananassae which affect almost exclusively the morphology and structure of the adult compound eye. These mutants, called Om for "optic morphology", appear as independent mutational events among the progeny of the ca;px stock or its derivatives. The Om mutants are semidominant, show few pleiotropic effects and have been assigned to at least 22 loci scattered in the genome. Hinton hypothesized that the Om mutability involved the presence of a transposable element which insertion is specific to some sequences shared by a group of genes that express coordinately during eye morphogenesis. These findings raise important questions as to the mechanism and specificity of the Om mutagenic effect. The Om mutations are caused by the insertion of a retrotransposon called tom (1,2,3). The tom element does not insert into the coding region of the genes that it mutates, but into adjacent sequences, without disrupting the signals necessary for transcription (2,4,5,6). Up to now, several Om mutants have been molecularly characterized. The Om(1D) expression is uniformly distributed in all the eye imaginal disc, however the expression is stronger in the differentiating photoreceptors preclusters posterior to the morphogenetic furrow (7). The tom element has been detected by in situ hybridization, in the preclusteers where it was found the Om(1D) gene expression. Om(1D) encodes a homeoprotein which is present seven times higher in the eye imaginal disc of the Om(1D) mutant than in the wild type. Tanda and Corces (7), proposed that a tissue-specific transcriptional enhancer present in the tom element, stimulate the expression of the Om(1D) gene when the tom element is inserted inclose proximity to it. There is evidence to suggest that Bar is the Drosophila melanogaster homologue of the Om(1D) gene (8,9). Awasaki et al. (4) found that the Om(1A) gene, is homologue to the cut homeoprotein gene of D. melanogaster (10). The Om(2D) mutant is of special interest because its gene product is not expressed in the wild type, however, it is found in the middle of the disc of the Om(2D)63 mutants, where excessive cell death occurs. It has been shown that the artificially induced ectopic expression of Om(2D) do not determine a Om(2D) phenotype (5). The aminoacidic sequence of the Om(2D) protein reveals a homeodomain that might be involved in transcription regulation events, however, its functional roll is still unknown. Yoshida and collaborators have proposed the involvement of an eye disc-specific regulatory factor present in the tom element to explain the Om(2D) gene expression only in these mutants. The Om suppressor mutants are as characteristic of the Om hypermutability system, as are the Om mutants themselves. Since all spontaneous suppressors have been found in the ca;px stock and its derivatives with the same frequency as that of Om mutations, it is thought that Om suppressors are also induced by tom element insertion (11). The studies on the Om(1J)Su locus and its function showed that the Om mutations can be suppressed by these gene. Using the in situ hybridization technique, with tom as probe, it was showed that the Om(1J)Su34 gene presents the tomelement at the position 6C on the left arm of the X chromosome, as it was suggested by Hinton (11) and verified by Matsubayashi (12). By using the "tom tagging" technique (13) 20 Kb of the Om(1J) locus region were cloned. The Northern blot analysis showed the presence of two transcripts (3.8 Kb and 2.4 Kb) within this cloned region, however, the in situ hybridization to the eye imaginal discs of wild type and mutants individuals did not show any differences in the expression. The Om suppression mechanism is now investigated by means of the genetic and molecular analyses of the revertants mutations of the Om(1J)Su34 suppressor gene. The obtained data permit an approach to the knowledge of the constitution of the Om(1J)Su region.
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[Cell Biology & Cytology] |
[Genetics & Bioinformatics] |
