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Genetic Interactions Between the Guanine Nucleotide Exchange Factor GEfmeso and GTPase signaling components in the drosophila wing reveal microenvironment dependent variation within gtpase signaling n

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Date Issued:
2012
Abstract/Description:
The Ras superfamily of GTPases are important regulators of morphogenesis involved in control of cytoskeletal dynamics, intracellular trafficking, apical-basal polarity and cell migration. Mis-regulation of GTPase signaling interferes with development and is linked to pathogenesis. Traditionally, GTPase signaling has been depicted as a series of independent linear pathways. However, recently it has become apparent that multiple GTPases can interact to regulate a single cellular process, functioning in poorly understood networks of cross talk between pathways during development. Jim Fristrom (unpublished data) identified a mutation (18-5) that interacts with components of the GTPases Rho1, Rala, and Cdc42 signaling in multiple developmental contexts. Genetic analysis, physical mapping studies, and sequencing of the mutant allele have indicated that the gene was an allele of GEFmeso (CG30115), which encodes guanine nucleotide exchange factor. To show that 18-5 is an allele of GEFmeso, I demonstrated that a GEFmeso transgene could functionally rescue developmental defects associated with the 18-5 mutation. I also investigated cross talk and network variation in signaling interactions between GEFmeso and other GTPase signaling components in the Drosophila wing. My data provide evidence for microenvironment-dependent variation in GTPase signaling networks in specific domains of the wing, and reveal intercellular variation in GTPase signaling within an otherwise uniform epithelium.
Title: Genetic Interactions Between the Guanine Nucleotide Exchange Factor GEfmeso and GTPase signaling components in the drosophila wing reveal microenvironment dependent variation within gtpase signaling n.
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Name(s): Iketani, Ashley, Author
Vonkalm, Laurence, Committee Chair
Stern, Michael, Committee Member
Fernandez-Valle, Cristina, Committee Member
, Committee Member
University of Central Florida, Degree Grantor
Type of Resource: text
Date Issued: 2012
Publisher: University of Central Florida
Language(s): English
Abstract/Description: The Ras superfamily of GTPases are important regulators of morphogenesis involved in control of cytoskeletal dynamics, intracellular trafficking, apical-basal polarity and cell migration. Mis-regulation of GTPase signaling interferes with development and is linked to pathogenesis. Traditionally, GTPase signaling has been depicted as a series of independent linear pathways. However, recently it has become apparent that multiple GTPases can interact to regulate a single cellular process, functioning in poorly understood networks of cross talk between pathways during development. Jim Fristrom (unpublished data) identified a mutation (18-5) that interacts with components of the GTPases Rho1, Rala, and Cdc42 signaling in multiple developmental contexts. Genetic analysis, physical mapping studies, and sequencing of the mutant allele have indicated that the gene was an allele of GEFmeso (CG30115), which encodes guanine nucleotide exchange factor. To show that 18-5 is an allele of GEFmeso, I demonstrated that a GEFmeso transgene could functionally rescue developmental defects associated with the 18-5 mutation. I also investigated cross talk and network variation in signaling interactions between GEFmeso and other GTPase signaling components in the Drosophila wing. My data provide evidence for microenvironment-dependent variation in GTPase signaling networks in specific domains of the wing, and reveal intercellular variation in GTPase signaling within an otherwise uniform epithelium.
Identifier: CFE0004252 (IID), ucf:49541 (fedora)
Note(s): 2012-05-01
M.S.
Sciences, Biology
Masters
This record was generated from author submitted information.
Subject(s): GTPase -- Cross talk -- Wing Veins
Persistent Link to This Record: http://purl.flvc.org/ucf/fd/CFE0004252
Restrictions on Access: campus 2013-05-15
Host Institution: UCF

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