Persistent Link:
http://hdl.handle.net/10150/244831
Title:
Modeling Heart Diseases in Drosophila
Author:
Swerdan, Stephanie
Issue Date:
May-2012
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

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleModeling Heart Diseases in Drosophilaen_US
dc.creatorSwerdan, Stephanieen_US
dc.contributor.authorSwerdan, Stephanieen_US
dc.date.issued2012-05-
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.abstractFragile 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.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.nameB.S.H.S.en_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
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