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    Modeling Heart Diseases in Drosophila

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    Author
    Swerdan, Stephanie
    Issue Date
    2012-05
    
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    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
    Fragile X mental retardation protein (FMRP) plays an important role in heart development and disease. Here we set out to create a Drosophila model of heart disease that will complement the existing mouse model based on Fragile X protein deficiency. Proteins within the Fragile X family are RNA binding proteins that control the translation of specific RNAs. Previous studies have shown that loss of Fragile X mental retardation protein, autosomal homolog 1 (FXR1) leads to heart phenotypes in the mouse. The Drosophila model will allow us to perform rapid genetic rescue experiments to identify specific targets of FMR1, the only type of FMR expressed in the fly, that are responsible for creating the structural and functional defects when FMR1 is repressed. To create a model of heart disease in the fly, we knocked down FMR1 and examined its effects by measuring the heart rate in early pupae. We discovered that the total loss of function for FMR1 leads a decreased heart rate. Interestingly, heterozygous loss of function (LOF) mutants exhibited a significant decrease in heart rate that could be partially rescued by inserting hFXR1, a human homolog of FMRP.
    Type
    text
    Electronic Thesis
    Degree Name
    B.S.H.S.
    Degree Level
    bachelors
    Degree Program
    Honors College
    Physiology
    Degree Grantor
    University of Arizona
    Collections
    Honors Theses

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