The small GTPase Rheb affects central brain neuronal morphology and memory formation in Drosophila
Mutations in either of two tumor suppressor genes, TSC1 or TSC2, cause tuberous sclerosis complex (TSC), a syndrome resulting in benign hamartomatous tumors and neurological disorders. Cellular growth defects and neuronal disorganization associated with TSC are believed to be due to upregulated TOR...
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| Veröffentlicht in: | PloS one 2012-09, Vol.7 (9), p.e44888-e44888 |
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| creator | Brown, Heather L D Kaun, Karla R Edgar, Bruce A |
| description | Mutations in either of two tumor suppressor genes, TSC1 or TSC2, cause tuberous sclerosis complex (TSC), a syndrome resulting in benign hamartomatous tumors and neurological disorders. Cellular growth defects and neuronal disorganization associated with TSC are believed to be due to upregulated TOR signaling. We overexpressed Rheb, an upstream regulator of TOR, in two different subsets of D. melanogaster central brain neurons in order to upregulate the Tsc-Rheb-TOR pathway. Overexpression of Rheb in either the mushroom bodies or the insulin producing cells resulted in enlarged axon projections and cell bodies, which continued to increase in size with prolonged Rheb expression as the animals aged. Additionally, Rheb overexpression in the mushroom bodies resulted in deficiencies in 3 hr but not immediate appetitive memory. Thus, Rheb overexpression in the central brain neurons of flies causes not only morphological phenotypes, but behavioral and aging phenotypes that may mirror symptoms of TSC. |
| doi_str_mv | 10.1371/journal.pone.0044888 |
| format | Article |
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Cellular growth defects and neuronal disorganization associated with TSC are believed to be due to upregulated TOR signaling. We overexpressed Rheb, an upstream regulator of TOR, in two different subsets of D. melanogaster central brain neurons in order to upregulate the Tsc-Rheb-TOR pathway. Overexpression of Rheb in either the mushroom bodies or the insulin producing cells resulted in enlarged axon projections and cell bodies, which continued to increase in size with prolonged Rheb expression as the animals aged. Additionally, Rheb overexpression in the mushroom bodies resulted in deficiencies in 3 hr but not immediate appetitive memory. Thus, Rheb overexpression in the central brain neurons of flies causes not only morphological phenotypes, but behavioral and aging phenotypes that may mirror symptoms of TSC.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0044888</identifier><identifier>PMID: 23028662</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Aging ; Aging - genetics ; Alzheimer's disease ; Animals ; Autophagy ; Biology ; Brain ; Brain - cytology ; Brain - metabolism ; Brain - physiology ; Brain research ; Cancer ; Cell cycle ; Cell growth ; Defects ; Dopamine ; Drosophila ; Drosophila melanogaster ; Drosophila melanogaster - cytology ; Drosophila melanogaster - metabolism ; Drosophila melanogaster - physiology ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Female ; Guanosine triphosphatases ; Insects ; Insulin ; Insulin-Secreting Cells - metabolism ; Kinases ; Male ; Medical research ; Memory ; Monomeric GTP-Binding Proteins - genetics ; Monomeric GTP-Binding Proteins - metabolism ; Morphology ; Mushroom bodies ; Mushroom Bodies - metabolism ; Mutation ; Mutation (Biology) ; Nervous system ; Nervous system diseases ; Neurological diseases ; Neurons ; Neurons - cytology ; Neurons - metabolism ; Neuropeptides - genetics ; Neuropeptides - metabolism ; Ras Homolog Enriched in Brain Protein ; Rodents ; Signaling ; Transcription Factors - genetics ; Tuberous sclerosis ; Tuberous Sclerosis Complex 1 ; Tuberous Sclerosis Complex 2 ; Tumor suppressor genes ; Tumors</subject><ispartof>PloS one, 2012-09, Vol.7 (9), p.e44888-e44888</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>Brown et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Brown et al 2012 Brown et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-573c4196cabf78c47b9da72d79a43f25e9f581da32653cc775dea1f573f3f12e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446999/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3446999/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23028662$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Singh, Shree Ram</contributor><creatorcontrib>Brown, Heather L D</creatorcontrib><creatorcontrib>Kaun, Karla R</creatorcontrib><creatorcontrib>Edgar, Bruce A</creatorcontrib><title>The small GTPase Rheb affects central brain neuronal morphology and memory formation in Drosophila</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Mutations in either of two tumor suppressor genes, TSC1 or TSC2, cause tuberous sclerosis complex (TSC), a syndrome resulting in benign hamartomatous tumors and neurological disorders. Cellular growth defects and neuronal disorganization associated with TSC are believed to be due to upregulated TOR signaling. We overexpressed Rheb, an upstream regulator of TOR, in two different subsets of D. melanogaster central brain neurons in order to upregulate the Tsc-Rheb-TOR pathway. Overexpression of Rheb in either the mushroom bodies or the insulin producing cells resulted in enlarged axon projections and cell bodies, which continued to increase in size with prolonged Rheb expression as the animals aged. Additionally, Rheb overexpression in the mushroom bodies resulted in deficiencies in 3 hr but not immediate appetitive memory. Thus, Rheb overexpression in the central brain neurons of flies causes not only morphological phenotypes, but behavioral and aging phenotypes that may mirror symptoms of TSC.</description><subject>Aging</subject><subject>Aging - genetics</subject><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Autophagy</subject><subject>Biology</subject><subject>Brain</subject><subject>Brain - cytology</subject><subject>Brain - metabolism</subject><subject>Brain - physiology</subject><subject>Brain research</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Defects</subject><subject>Dopamine</subject><subject>Drosophila</subject><subject>Drosophila melanogaster</subject><subject>Drosophila melanogaster - cytology</subject><subject>Drosophila melanogaster - metabolism</subject><subject>Drosophila melanogaster - physiology</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Female</subject><subject>Guanosine triphosphatases</subject><subject>Insects</subject><subject>Insulin</subject><subject>Insulin-Secreting Cells - 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genetics</topic><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Autophagy</topic><topic>Biology</topic><topic>Brain</topic><topic>Brain - cytology</topic><topic>Brain - metabolism</topic><topic>Brain - physiology</topic><topic>Brain research</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Defects</topic><topic>Dopamine</topic><topic>Drosophila</topic><topic>Drosophila melanogaster</topic><topic>Drosophila melanogaster - cytology</topic><topic>Drosophila melanogaster - metabolism</topic><topic>Drosophila melanogaster - physiology</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Female</topic><topic>Guanosine triphosphatases</topic><topic>Insects</topic><topic>Insulin</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>Medical research</topic><topic>Memory</topic><topic>Monomeric GTP-Binding Proteins - genetics</topic><topic>Monomeric GTP-Binding Proteins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Heather L D</au><au>Kaun, Karla R</au><au>Edgar, Bruce A</au><au>Singh, Shree Ram</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The small GTPase Rheb affects central brain neuronal morphology and memory formation in Drosophila</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-09-19</date><risdate>2012</risdate><volume>7</volume><issue>9</issue><spage>e44888</spage><epage>e44888</epage><pages>e44888-e44888</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Mutations in either of two tumor suppressor genes, TSC1 or TSC2, cause tuberous sclerosis complex (TSC), a syndrome resulting in benign hamartomatous tumors and neurological disorders. Cellular growth defects and neuronal disorganization associated with TSC are believed to be due to upregulated TOR signaling. We overexpressed Rheb, an upstream regulator of TOR, in two different subsets of D. melanogaster central brain neurons in order to upregulate the Tsc-Rheb-TOR pathway. Overexpression of Rheb in either the mushroom bodies or the insulin producing cells resulted in enlarged axon projections and cell bodies, which continued to increase in size with prolonged Rheb expression as the animals aged. Additionally, Rheb overexpression in the mushroom bodies resulted in deficiencies in 3 hr but not immediate appetitive memory. Thus, Rheb overexpression in the central brain neurons of flies causes not only morphological phenotypes, but behavioral and aging phenotypes that may mirror symptoms of TSC.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23028662</pmid><doi>10.1371/journal.pone.0044888</doi><tpages>e44888</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging Aging - genetics Alzheimer's disease Animals Autophagy Biology Brain Brain - cytology Brain - metabolism Brain - physiology Brain research Cancer Cell cycle Cell growth Defects Dopamine Drosophila Drosophila melanogaster Drosophila melanogaster - cytology Drosophila melanogaster - metabolism Drosophila melanogaster - physiology Drosophila Proteins - genetics Drosophila Proteins - metabolism Female Guanosine triphosphatases Insects Insulin Insulin-Secreting Cells - metabolism Kinases Male Medical research Memory Monomeric GTP-Binding Proteins - genetics Monomeric GTP-Binding Proteins - metabolism Morphology Mushroom bodies Mushroom Bodies - metabolism Mutation Mutation (Biology) Nervous system Nervous system diseases Neurological diseases Neurons Neurons - cytology Neurons - metabolism Neuropeptides - genetics Neuropeptides - metabolism Ras Homolog Enriched in Brain Protein Rodents Signaling Transcription Factors - genetics Tuberous sclerosis Tuberous Sclerosis Complex 1 Tuberous Sclerosis Complex 2 Tumor suppressor genes Tumors |
| title | The small GTPase Rheb affects central brain neuronal morphology and memory formation in Drosophila |
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