Font Size: a A A

Impact On Drosophila Brain Developement Through The Overexpression And Loss Of Function Of Gsα

Posted on:2011-09-07Degree:MasterType:Thesis
Country:ChinaCandidate:W C JiangFull Text:PDF
GTID:2210330362453252Subject:Biology
Abstract/Summary:PDF Full Text Request
G protein signalling pathway is an important siganalling pathway of cells. This pathway participates in a variety of regulations such as transcription of genes, cell proliferation and so on. The G protein complex consists of three subunits namedα,β,γrespectively.Gαis the most important one of these three subunits. Gαtransduces external signals through the cAMP-PKA signaling pathway. Research shows the mutation of Gαsubunit affacts the activity of ion channels of cells. And it also influences the mitotic spindle orientation of neuroblasts and the asymmetric division of neuroblasts in Drosophila. But there are no reports as yet concerning the impact of Gsαon the development of Drosophila brain.To investigate the Gsαfunction in the development of Drosophila brain, we designed the overexpression and loss of function experiments of Gsα. We overexpressed Gsαthrough the GAL4-UAS system. And hsGAL4-UAS system helped us to learn the impact of transient and mass expression of Gsαon the development of Drosophila brain. We also used FLP-out system to investigate whether the overexpression of Gsαin a sub-area will affact cell fates. In the same way, we investigated the influence of the loss of function of Gsαin terms of Drosophila development through somatic cell clone technology.The results showed that the overexpression of Gsαwas lethal to Drosophila larva both in 25 centigrade and 31 centigrade. The fate of individual cells of Drosophila brain changed in the hsGAL4-UAS experiment. And the loss of function of Gsαin the Drosophila brain did not seem to affact the cell fate of Drosophila brain and did not interfere the cell cycles of Drosophila brain cells.
Keywords/Search Tags:G protein, signalling pathway, Gsαoverexpression, loss of funtion
PDF Full Text Request
Related items