THESIS
2017
viii, 44 pages : color illustrations ; 30 cm
Abstract
Cell competition is an intrinsic tissue surveillance mechanism that functions to eliminate unfit
cells. Loss of cell polarity can trigger cell competition. The Scribble polarity complex, which
is located at the basolateral region of epithelial cells, is a well-established model to study cell
competition. The Scribble complex is composed of three proteins: Scribble (Scrib), Discs-Large (Dlg) and Lethal giant larvae (Lgl). Homozygous mutants of the Scribble group genes
lead to lethal and invasive tumor formation. When the scribble or dlg mutant cells are
generated as mosaic clones, these mutant cells undergo cell competition-induced apoptosis.
In order to identify the molecular network that regulates the elimination of scribble mutant
cells during cell competition, we compared the...[
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Cell competition is an intrinsic tissue surveillance mechanism that functions to eliminate unfit
cells. Loss of cell polarity can trigger cell competition. The Scribble polarity complex, which
is located at the basolateral region of epithelial cells, is a well-established model to study cell
competition. The Scribble complex is composed of three proteins: Scribble (Scrib), Discs-Large (Dlg) and Lethal giant larvae (Lgl). Homozygous mutants of the Scribble group genes
lead to lethal and invasive tumor formation. When the scribble or dlg mutant cells are
generated as mosaic clones, these mutant cells undergo cell competition-induced apoptosis.
In order to identify the molecular network that regulates the elimination of scribble mutant
cells during cell competition, we compared the transcriptomes of imaginal discs harboring
scribble mutant clones and those harboring control clones. We identified that Down syndrome
cell adherin molecule 4 (Dscam4) was significantly upregulted in imaginal discs harboring
scribble mutant clones in comparison with those bearing control clones. We further found that
depletion of Dscam4 could rescue scribble mutant cells from elimination. DSCAM family
proteins are known as neuronal recognition molecules that mediate self-avoidance during
dentrite tiling. Here we identified a novel role of Dscam4 in the epithelia to maintain tissue
fitness.
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