THESIS
2018
viii, 1, 71 pages : color illustrations ; 30 cm
Abstract
In Drosophila, epithelial tissues with homozygous mutant for any of the neoplastic tumor
suppressor genes (nTSGs), including Scrib, Dlg and Lgl, will lose epithelial structures and form
amorphous tumors. However, when these nTSGs mutant cells are confronted with normal cells,
a cell competition process lead to elimination of nTSGs mutant cells. The JNK, Hippo, Notch
and EGFR signaling pathways have been reported to play a role in regulating Scrib mutation-induced
cell competition. We found that modulation of these signaling pathways will rescue
Scrib-depleted cells from cell competition-induced elimination and promote tumor overgrowth,
include blockage of JNK signaling through overexpressing Bsk
DN, activation of Yki activity
through overexpressing Yki or YkiS168A, activation of...[
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In Drosophila, epithelial tissues with homozygous mutant for any of the neoplastic tumor
suppressor genes (nTSGs), including Scrib, Dlg and Lgl, will lose epithelial structures and form
amorphous tumors. However, when these nTSGs mutant cells are confronted with normal cells,
a cell competition process lead to elimination of nTSGs mutant cells. The JNK, Hippo, Notch
and EGFR signaling pathways have been reported to play a role in regulating Scrib mutation-induced
cell competition. We found that modulation of these signaling pathways will rescue
Scrib-depleted cells from cell competition-induced elimination and promote tumor overgrowth,
include blockage of JNK signaling through overexpressing Bsk
DN, activation of Yki activity
through overexpressing Yki or YkiS168A, activation of EGFR signaling activity through
overexpressing Ras
V12 and activation of Notch signaling through overexpressing NICD. To
dissect whether and how these signaling pathways affect the growth outcome of Scrib-depleted
cell clones, we performed transcriptome analysis of these tumors with signaling pathway
modulations. These data will allow us to systematically map the Ras, Notch, Hippo and JNK
signaling network in the drosophila nTSG tumor growth model and identify key codes in the
network determining the growth outcome of nTSG mutant cells.
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