Regulation of Epithelial Morphogenesis by the Drosophila Folded gastrulation Signaling Pathway Public Deposited

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  • March 20, 2019
  • Manning, Alyssa Julia
    • Affiliation: College of Arts and Sciences, Department of Biology
  • Understanding morphogenesis, the set of processes by which cells are rearranged and change shape to form organs and other higher-order structures, is crucial to our knowledge of biology. I have used the Folded gastrulation (Fog) signaling pathway necessary for Drosophila epithelial folding to study the principles of morphogenesis. During gastrulation, a signal from the secreted protein Fog is received by cells of the presumptive mesoderm. Then the Gα protein, Concertina (Cta), signals through the canonical Rho axis to induce actin-based apical constriction and invagination of these cells. This pathway is also active during several other epithelial folding events throughout development. We have developed a cell culture model to study Fog signaling and used it to discover a GPCR, Mist, which is a Fog receptor. mist RNA is specifically expressed in cells known to undergo Fog signaling. We show that the transcription factor Snail is necessary for mist expression in the mesoderm. We have also made a deletion allele which disrupts mist expression. This allele causes ventral midline defects and improper invagination of mesodermal cells, which shows that mist is also required for proper gastrulation movements. We also investigated GPRK2 and Kurtz which act as negative regulators of Mist signaling in cell culture. Alterations of Kurtz levels in wing discs disrupt their folding, similarly to core Fog pathway components. These data reveal that the GPCR Mist controls the location and timing of epithelial morphogenesis in Drosophila downstream of Fog.
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  • In Copyright
  • Rogers, Stephen
  • Doctor of Philosophy
Graduation year
  • 2013

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