Persistent Link:
http://hdl.handle.net/10150/195589
Title:
Translational Control of Synaptic Plasticity
Author:
Cziko, Anne-Marie
Issue Date:
2009
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Activity-dependent and synapse-specific translation of mRNAs is required for long-term changes in synaptic strength (or efficacy). However, many of the components mediating repression, transport and activation of mRNAs are unknown. Translational control in neurons is a highly conserved process and mediated by a ribonuclear particle (RNP). This study shows that RNPs in Drosophila neurons are similar not only to mammalian neuronal RNA granules but also to yeast P-bodies, cytoplasmic foci involved in translational repression and RNA decay. The evolutionarily conserved proteins Me31b and Trailer Hitch localize to RNA granules. Me31b and Trailer Hitch are required for normal dendritic growth. Mutations in Me31b and Trailer Hitch suppress phenotypes resulting from overexpression of Fragile X Mental Retardation protein, suggesting that both proteins may act as translational repressors. In addition, this study reports the identification of novel translational repressors in neurons. Using the overexpression phenotype of Fragile X Mental Retardation protein in a candidate-based genetic screen, I identified dominant suppressor mutations in five genes, including Doubletime/Discs Overgrown, Orb2/CPEB, PolyA Binding Protein, Rm62/Dmp68 and SmD3. Like Me31b and Trailer Hitch, all five proteins localize to neuronal RNPs. Overexpression of each proteins affects dendritic branching of sensory neurons in Drosophila. Identification and further characterization of these novel RNP granule components and dFMR1-interacting proteins may provide further insights into the mechanisms controlling translational in dendrites.
Type:
text; Electronic Dissertation
Keywords:
candidate based screen; dendrites; Drosophila; neurons; synaptic plasticity; translational control
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Neuroscience; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Zinsmaier, Konrad E.
Committee Chair:
Zinsmaier, Konrad E.

Full metadata record

DC FieldValue Language
dc.language.isoENen_US
dc.titleTranslational Control of Synaptic Plasticityen_US
dc.creatorCziko, Anne-Marieen_US
dc.contributor.authorCziko, Anne-Marieen_US
dc.date.issued2009en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractActivity-dependent and synapse-specific translation of mRNAs is required for long-term changes in synaptic strength (or efficacy). However, many of the components mediating repression, transport and activation of mRNAs are unknown. Translational control in neurons is a highly conserved process and mediated by a ribonuclear particle (RNP). This study shows that RNPs in Drosophila neurons are similar not only to mammalian neuronal RNA granules but also to yeast P-bodies, cytoplasmic foci involved in translational repression and RNA decay. The evolutionarily conserved proteins Me31b and Trailer Hitch localize to RNA granules. Me31b and Trailer Hitch are required for normal dendritic growth. Mutations in Me31b and Trailer Hitch suppress phenotypes resulting from overexpression of Fragile X Mental Retardation protein, suggesting that both proteins may act as translational repressors. In addition, this study reports the identification of novel translational repressors in neurons. Using the overexpression phenotype of Fragile X Mental Retardation protein in a candidate-based genetic screen, I identified dominant suppressor mutations in five genes, including Doubletime/Discs Overgrown, Orb2/CPEB, PolyA Binding Protein, Rm62/Dmp68 and SmD3. Like Me31b and Trailer Hitch, all five proteins localize to neuronal RNPs. Overexpression of each proteins affects dendritic branching of sensory neurons in Drosophila. Identification and further characterization of these novel RNP granule components and dFMR1-interacting proteins may provide further insights into the mechanisms controlling translational in dendrites.en_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.subjectcandidate based screenen_US
dc.subjectdendritesen_US
dc.subjectDrosophilaen_US
dc.subjectneuronsen_US
dc.subjectsynaptic plasticityen_US
dc.subjecttranslational controlen_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineNeuroscienceen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorZinsmaier, Konrad E.en_US
dc.contributor.chairZinsmaier, Konrad E.en_US
dc.contributor.committeememberWilson, Jeanen_US
dc.contributor.committeememberParker, Roy R.en_US
dc.identifier.proquest10489en_US
dc.identifier.oclc659752194en_US
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