Ectopic expression of mnb and Hip1 alters Drosophila development
Thesis (M.Sc.)--Memorial University of Newfoundland, 2009. Biology Includes bibliographical references (leaves 96-105) A powerful approach to studying the mechanisms of disease is through the use of transgenic models like Drosophila melanogaster. The Drosophila homologue of the human Down syndrome c...
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ftmemorialunivdc:oai:collections.mun.ca:theses4/50097 2023-05-15T17:23:33+02:00 Ectopic expression of mnb and Hip1 alters Drosophila development MacDonald, Jillian M. (Jillian Michelle). Memorial University of Newfoundland. Dept. of Biology 2008. xi, 106 leaves : ill. (chiefly col) Image/jpeg; Application/pdf http://collections.mun.ca/cdm/ref/collection/theses4/id/50097 Eng eng Electronic Theses and Dissertations (12.07 MB) -- http://collections.mun.ca/PDFs/theses/MacDonald_Jillian.pdf a3242040 http://collections.mun.ca/cdm/ref/collection/theses4/id/50097 The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. Paper copy kept in the Centre for Newfoundland Studies, Memorial University Libraries Developmental neurobiology Drosophila melanogaster--Growth Protein kinases Protein-protein interactions Proteins--Physiological effect Text Electronic thesis or dissertation 2008 ftmemorialunivdc 2015-08-06T19:21:57Z Thesis (M.Sc.)--Memorial University of Newfoundland, 2009. Biology Includes bibliographical references (leaves 96-105) A powerful approach to studying the mechanisms of disease is through the use of transgenic models like Drosophila melanogaster. The Drosophila homologue of the human Down syndrome candidate gene, Dyrk1A, is minibrain (mnb). Studies have shown that mnb can participate in development of the Drosophila eye to control growth and survival through modification of insulin receptor signalling. Huntingtin-interacting protein 1 (Hip1), which differentially interacts with the mutant and normal forms of the Huntington disease protein, huntingtin, has been shown to play a role in Drosophila neurogenesis. There are two naturally occurring versions of the Hip1 protein, a full length version and a truncated version missing the N-terminal ANTH domain, referred to as Hip1ΔANTH. As a biochemical interaction has been identified between Hip1 and Dyrk1A/mnb, this study examines these two genes in Drosophila development. In this study the UAS-Ga14 system was utilized to direct the expression of Dyrk1A/mnb, Hip1 and components of the insulin signalling pathway, akt & foxo1, in the developing dorsal notum and eye. While neither mnb nor foxo1 over-expression has any effect, we found that over-expression of akt, a component of the insulin signalling pathway, increases the microchaetae density on the dorsal notum. The over-expression of mnb and Hip1 in the eye have no effect on eye development. Under the sensitized growth conditions where the GMRGa14 also drives the UASfoxo11 transgene, the full length versions of Hip1 show decreased bristle number and decreased ommatidia number while the truncated versions of Hip1 lacking the lipid-binding ANTH domain show decreased ommatidia number. Over-expression of mnb and Hip1 together with foxo1 show changes in eye development, indicating a possible interaction between these two genes. As these are genes in two completely different diseases, finding how they interact could provide a key insight into finding therapies for neurodegenerative diseases. Thesis Newfoundland studies University of Newfoundland Memorial University of Newfoundland: Digital Archives Initiative (DAI) Huntington ENVELOPE(-127.078,-127.078,54.707,54.707) |
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Memorial University of Newfoundland: Digital Archives Initiative (DAI) |
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ftmemorialunivdc |
language |
English |
topic |
Developmental neurobiology Drosophila melanogaster--Growth Protein kinases Protein-protein interactions Proteins--Physiological effect |
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Developmental neurobiology Drosophila melanogaster--Growth Protein kinases Protein-protein interactions Proteins--Physiological effect MacDonald, Jillian M. (Jillian Michelle). Ectopic expression of mnb and Hip1 alters Drosophila development |
topic_facet |
Developmental neurobiology Drosophila melanogaster--Growth Protein kinases Protein-protein interactions Proteins--Physiological effect |
description |
Thesis (M.Sc.)--Memorial University of Newfoundland, 2009. Biology Includes bibliographical references (leaves 96-105) A powerful approach to studying the mechanisms of disease is through the use of transgenic models like Drosophila melanogaster. The Drosophila homologue of the human Down syndrome candidate gene, Dyrk1A, is minibrain (mnb). Studies have shown that mnb can participate in development of the Drosophila eye to control growth and survival through modification of insulin receptor signalling. Huntingtin-interacting protein 1 (Hip1), which differentially interacts with the mutant and normal forms of the Huntington disease protein, huntingtin, has been shown to play a role in Drosophila neurogenesis. There are two naturally occurring versions of the Hip1 protein, a full length version and a truncated version missing the N-terminal ANTH domain, referred to as Hip1ΔANTH. As a biochemical interaction has been identified between Hip1 and Dyrk1A/mnb, this study examines these two genes in Drosophila development. In this study the UAS-Ga14 system was utilized to direct the expression of Dyrk1A/mnb, Hip1 and components of the insulin signalling pathway, akt & foxo1, in the developing dorsal notum and eye. While neither mnb nor foxo1 over-expression has any effect, we found that over-expression of akt, a component of the insulin signalling pathway, increases the microchaetae density on the dorsal notum. The over-expression of mnb and Hip1 in the eye have no effect on eye development. Under the sensitized growth conditions where the GMRGa14 also drives the UASfoxo11 transgene, the full length versions of Hip1 show decreased bristle number and decreased ommatidia number while the truncated versions of Hip1 lacking the lipid-binding ANTH domain show decreased ommatidia number. Over-expression of mnb and Hip1 together with foxo1 show changes in eye development, indicating a possible interaction between these two genes. As these are genes in two completely different diseases, finding how they interact could provide a key insight into finding therapies for neurodegenerative diseases. |
author2 |
Memorial University of Newfoundland. Dept. of Biology |
format |
Thesis |
author |
MacDonald, Jillian M. (Jillian Michelle). |
author_facet |
MacDonald, Jillian M. (Jillian Michelle). |
author_sort |
MacDonald, Jillian M. (Jillian Michelle). |
title |
Ectopic expression of mnb and Hip1 alters Drosophila development |
title_short |
Ectopic expression of mnb and Hip1 alters Drosophila development |
title_full |
Ectopic expression of mnb and Hip1 alters Drosophila development |
title_fullStr |
Ectopic expression of mnb and Hip1 alters Drosophila development |
title_full_unstemmed |
Ectopic expression of mnb and Hip1 alters Drosophila development |
title_sort |
ectopic expression of mnb and hip1 alters drosophila development |
publishDate |
2008 |
url |
http://collections.mun.ca/cdm/ref/collection/theses4/id/50097 |
long_lat |
ENVELOPE(-127.078,-127.078,54.707,54.707) |
geographic |
Huntington |
geographic_facet |
Huntington |
genre |
Newfoundland studies University of Newfoundland |
genre_facet |
Newfoundland studies University of Newfoundland |
op_source |
Paper copy kept in the Centre for Newfoundland Studies, Memorial University Libraries |
op_relation |
Electronic Theses and Dissertations (12.07 MB) -- http://collections.mun.ca/PDFs/theses/MacDonald_Jillian.pdf a3242040 http://collections.mun.ca/cdm/ref/collection/theses4/id/50097 |
op_rights |
The author retains copyright ownership and moral rights in this thesis. Neither the thesis nor substantial extracts from it may be printed or otherwise reproduced without the author's permission. |
_version_ |
1766113243622801408 |