The Sonic hedgehog (Shh) signaling pathway plays a critical role in murine gastric
development. When Shh is knocked out in the mouse embryonic stomach, glandular epithelial
hyperplasia occurs. Furthermore, this phenotype was mimicked in Gli3−/−, but not Gli2−/− stomachs. I utilized three additional mouse models that modulate Gli3 activity to better understand the role of Gli3 in the developing stomach - the Gli3Δ699/Δ699 ,Gli3P1−4/P1−4, and Kif7−/−
mice. The Gli3P1−4/P1−4 stomach displayed glandular epithelial overgrowth, as did the Kif7−/− stomach to a lesser extent; the Gli3Δ699/Δ699 stomach displayed glandular hypoplasia. Moreover, the Gli3P1−4/P1−4 and Kif7−/− stomachs have a thicker circular smooth muscle, and the Gli3Δ699/Δ699 had a thinner one relative to wild-type. It appears that altering the balance of Gli3 in favour of its activator results in gastric glandular epithelial and circular smooth muscle hyperplasia, and a balance favouring the Gli3 repressor results in hypoplasia.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/32234 |
| Date | 21 March 2012 |
| Creators | Choi, Ruth |
| Contributors | Kim, Peter |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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