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    Genomic Approaches to Identifying Transcriptional Targets of AP-1, CREB and JNK Signaling in the Nervous System of Drosophila melanogaster

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    Author
    Etter, Paul Dezso
    Issue Date
    2005
    Keywords
    Molecular & Cellular Biology
    Advisor
    Ramaswami, Mani
    Committee Chair
    Ramaswami, Mani
    
    Metadata
    Show full item record
    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
    Although a few regulators of memory and addiction have been identified, the biochemical pathways that mediate the development of addiction and memory remain poorly understood. In addition, important questions remain as to how these two phenomena can persist for so long, sometimes for the entire life of an individual.Signaling molecules and transcription factors are activated in response to stimuli that induce long-term neuronal plastic changes. The transcription factor CREB (cAMP-responsive element binding protein) is clearly involved in triggering processes of addiction and memory, but its sustained activation following a course of chronic drug exposure (or learning) returns to baseline within days [1]. Even the enduring increased levels of deltaFosB (a Fos family transcription factor that couples with other proteins in the AP-1 family to form transcriptional activator/repressor complexes) observed in regions of the mammalian brain following chronic drug exposure, persists for only weeks or months. Thus, although CREB and deltaFosB probably initiate the very stable behavioral changes seen with addiction and memory, their alterations cannot mediate those behavioral changes per se [1]. Long-term up- or down-regulation of molecules downstream of these transcription factors, or others, must be responsible for the enduring modifications in synaptic connectivity and structure believed to be required for the maintenance of these durable behavioral states [2].Many believe that more rapid progress will be made toward understanding the molecular basis of addiction if research efforts proceed hand-in-hand with, rather than in isolation from, the overlapping neurobiological study of learning and memory [1, 2]. The importance and utility of using simple model systems such as Drosophila and Aplysia to identify and characterize genes involved in long-term synaptic plasticity, and hence memory formation, is well documented [3-5]. Identification and functional analyses of neuronal genes transcriptionally regulated by AP-1 and CREB in Drosophila would elaborate on molecular mechanisms of long-term plasticity and hence help us understand, and perhaps manipulate, processes that underlie addiction and memory.
    Type
    text
    Electronic Dissertation
    Degree Name
    PhD
    Degree Level
    doctoral
    Degree Program
    Molecular & Cellular Biology
    Graduate College
    Degree Grantor
    University of Arizona
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    Dissertations

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