The effect of Apc on Wnt Signaling in the Dorsal Telencephalon of Mus muscullis
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Authors
Maganti, Jansi
Issue Date
2008
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
The adenomatous polyposis coli (Apc) gene is known to encode the APC protein, a
component of the Wnt signaling pathway that causes the degradation of π½-catenin. A previous
study by the lab of Dr. Yuan Zhu generated Mus musculus (mice) expressing nonfunctional Apc
that was truncated (floxed) through use of the Cre/lox-P system. Apc flox/flox hGFAP-Cre + mutants
presented with cortical defects as well as increased π½-catenin levels in clumps of neural
precursor-like cells. It was hypothesized that defunct Apc caused accumulation of π½-catenin in
the brain, leading to aberrant Wnt signaling and causing the defects. The current study tested this
hypothesis by breeding mutants with mutations in both the Apc and π½-catenin genes. Brain
morphology was analyzed at post-natal day 0.5 using H&E staining as well as
immunohistochemistry labeling neural precursor cells and cortical layers. Because Apc flox/flox π½-cat flox/flox hGFAP-Cre + mutants appeared to recover from the defects, it was concluded that the original phenotype was caused by changes in Wnt signaling due to defunct Apc. However, these
mice presented a phenotype that was not consistent with' that of controls . Apc flox/+ π½cat flox/flox
hGFAP-Cre+ mutants presented similarly, suggesting a phenotype associated with π½-catenin loss.
Apc flox/+ π½-cat flox/+ hGFAP-Cre + mutants appeared phenotypically normal. Apc flox/+ π½-cat flox/+
hGFAP-Cre + showed a gradation of phenotypes. It was determined that the defects in Apc flox/flox
hGFAP-Cre + mutants were due to π½-catenin accumulation in the telencephalon, however the
phenotype presented by π½cat flox/flox hGFAP-Cre + mutants was of interest and will be studied in
the future.
Description
v, 40 p.
Citation
Publisher
Kalamazoo College
License
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