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The role of Gliotactin in planar cell polarity Venema, Dennis Roy
Abstract
Epithelial sheets exhibit apical-basal polarity and may also be polarized within the plane of the epithelium, a feature known as planar cell polarity, or PCP. In Drosophila, the pleated septate junction is a basolateral cell-cell junction that contributes to apicalbasal polarity. Gliotactin is a transmembrane protein with homology to serine esterases that localizes to the septate junction at the common vertex of three adjoining cells. Gliotactin is necessary for the function of the embryonic blood-nerve barrier which is formed by glial-glial septate junctions, as well as for septate junction formation in the embryonic epidermis. While septate junctions are a ubiquitous feature of epithelial sheets in Drosophila, the role of Gliotactin in post-embryonic tissues has not been addressed. In this thesis the role of Gliotactin in the development of polarized post-embyronic epithelia was investigated. The Drosophila wing epithelium has both apical-basal and planar polarity. Through mutant analysis it was demonstrated that Gliotactin is required for PCP in this epithelium. The Gliotactin wing PCP phenotype was sensitive to enhancement by the septate-junction mutants scribble, discs-large, coracle and Neurexin IV, and by the putative septate-junction mutant vulcan. Through genetic tests these mutations were found to function in the Gliotactin PCP pathway in epistasis groups consistent with previous work in the embyonic epidermis. Combinatorial septate-junction mutations were found to cause blisters at the wing margin, identifying a role for Gliotactin and other septate-junction components in adhesion between wing epithelial layers. The Gliotactin PCP pathway was shown to be independent of the frizzled PCP signaling pathway through cell biological and genetic assays. Finally, a novel component of the Gliotactin pathway was identified through a genetic screen for modifiers of Gliotactin PCP phenotypes. A model of Gliotactin function in/h'zz/ed-independent PCP in the wing is presented.
Item Metadata
Title |
The role of Gliotactin in planar cell polarity
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Creator | |
Publisher |
University of British Columbia
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Date Issued |
2003
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Description |
Epithelial sheets exhibit apical-basal polarity and may also be polarized within the
plane of the epithelium, a feature known as planar cell polarity, or PCP. In Drosophila,
the pleated septate junction is a basolateral cell-cell junction that contributes to apicalbasal
polarity. Gliotactin is a transmembrane protein with homology to serine esterases
that localizes to the septate junction at the common vertex of three adjoining cells.
Gliotactin is necessary for the function of the embryonic blood-nerve barrier which is
formed by glial-glial septate junctions, as well as for septate junction formation in the
embryonic epidermis. While septate junctions are a ubiquitous feature of epithelial sheets
in Drosophila, the role of Gliotactin in post-embryonic tissues has not been addressed.
In this thesis the role of Gliotactin in the development of polarized post-embyronic
epithelia was investigated. The Drosophila wing epithelium has both apical-basal and
planar polarity. Through mutant analysis it was demonstrated that Gliotactin is required
for PCP in this epithelium. The Gliotactin wing PCP phenotype was sensitive to
enhancement by the septate-junction mutants scribble, discs-large, coracle and Neurexin
IV, and by the putative septate-junction mutant vulcan. Through genetic tests these
mutations were found to function in the Gliotactin PCP pathway in epistasis groups
consistent with previous work in the embyonic epidermis. Combinatorial septate-junction
mutations were found to cause blisters at the wing margin, identifying a role for
Gliotactin and other septate-junction components in adhesion between wing epithelial
layers. The Gliotactin PCP pathway was shown to be independent of the frizzled PCP
signaling pathway through cell biological and genetic assays. Finally, a novel component
of the Gliotactin pathway was identified through a genetic screen for modifiers of
Gliotactin PCP phenotypes. A model of Gliotactin function in/h'zz/ed-independent PCP
in the wing is presented.
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Extent |
10985327 bytes
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Genre | |
Type | |
File Format |
application/pdf
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Language |
eng
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Date Available |
2009-11-11
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Provider |
Vancouver : University of British Columbia Library
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Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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DOI |
10.14288/1.0091304
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
2003-05
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Campus | |
Scholarly Level |
Graduate
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Aggregated Source Repository |
DSpace
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Item Citations and Data
Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.