A Systematic Screen for Human Genes Involved in Cell Migration by Mis-expression in Drosophila melanogaster

碩士 === 長庚大學 === 基礎醫學研究所 === 93 === The discovery of gene functions is a main theme in the post-genomic era. In this project, Drosophila melanogaster was used as an animal model to study the function of novel genes, since many regulatory mechanisms of signal transduction are highly conserved in Dros...

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Bibliographic Details
Main Authors: Ta-Shun Liao, 廖大勳
Other Authors: Li-Mei Pai
Format: Others
Language:en_US
Published: 2005
Online Access:http://ndltd.ncl.edu.tw/handle/33731986589372765115
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Summary:碩士 === 長庚大學 === 基礎醫學研究所 === 93 === The discovery of gene functions is a main theme in the post-genomic era. In this project, Drosophila melanogaster was used as an animal model to study the function of novel genes, since many regulatory mechanisms of signal transduction are highly conserved in Drosophila and humans. Using the UAS-Gal4 system, the human cDNAs were ectopically overexpressed in the Drosophila follicle cells, border cells, and wing. To examine whether the human cDNAs were involved in the epidermal growth factor receptor (EGFR) signaling pathway, they were overexpressed in the wings in the cbl (a negative regulator of EGFR) sensitized background. Totally 33 genes with 104 transgenic fly lines have been assayed. In this functional screen, it was found that 3 genes were involved in wing vein formation, one gene in the regulatory mechanism of EGFR signaling, and 5 genes caused delaying effect on the border-cell migration. Among genes causing defects in border-cell migration, KIAA1335 was found to regulate the DE-cadherin in the border-cell cluster. Another gene, FLJ11252, which had been found overexpressed in hepatocellular carcinoma, seemed to promote the cell motility of MDCK cells in the transwell assay. When expressed in MDCK cells, FLJ11252 were found enriched and localized at the cell membrane. This gave a cue that this gene might increase the cell motility by regulating the organization of cytoskeleton.