Presentation Title

Impact of a Akap200 Homozygous Null Mutant on Frizzled-independent Planar Cell Polarity in the Drosophila Wing Epithelium

Format of Presentation

Poster to be presented Friday March 31, 2017

Abstract

In the Drosophila wing epithelium, tissue (planar) polarity is controlled by the frizzled-signalling pathway and a second, frizzled-independent, signalling pathway. While the frizzled pathway controls global polarity, the frizzled-independent pathway regulates local cell polarity, resulting in parallel alignment of the epithelial cell wing hairs. The frizzled-independent pathway is regulated by many septate junction proteins, including neurexin IV, discs large, gliotactin, coracle, and scribble, and disruption of this pathway produces misaligned wing hairs. A forward mutagenesis approach was employed in Drosophila with a hypomorphic gliotactin background to identify new proteins that, when disrupted, contribute to the wing hair misalignment phenotype. Through this method, the non-septate junction protein Akap200 was identified as a component of the frizzled-independent pathway. This study examined a homozygous Akap200 null mutant and found that it is characterized by reduced viability and wing hair misalignment. Analysis under confocal fluorescence microscopy revealed that in the homozygous mutant, Akap200 fails to localize apically within the wing epithelium and remains diffuse in the tissue throughout development.

Department

Biological Sciences

Faculty Advisor

Dennis Venema

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Impact of a Akap200 Homozygous Null Mutant on Frizzled-independent Planar Cell Polarity in the Drosophila Wing Epithelium

In the Drosophila wing epithelium, tissue (planar) polarity is controlled by the frizzled-signalling pathway and a second, frizzled-independent, signalling pathway. While the frizzled pathway controls global polarity, the frizzled-independent pathway regulates local cell polarity, resulting in parallel alignment of the epithelial cell wing hairs. The frizzled-independent pathway is regulated by many septate junction proteins, including neurexin IV, discs large, gliotactin, coracle, and scribble, and disruption of this pathway produces misaligned wing hairs. A forward mutagenesis approach was employed in Drosophila with a hypomorphic gliotactin background to identify new proteins that, when disrupted, contribute to the wing hair misalignment phenotype. Through this method, the non-septate junction protein Akap200 was identified as a component of the frizzled-independent pathway. This study examined a homozygous Akap200 null mutant and found that it is characterized by reduced viability and wing hair misalignment. Analysis under confocal fluorescence microscopy revealed that in the homozygous mutant, Akap200 fails to localize apically within the wing epithelium and remains diffuse in the tissue throughout development.