The effect of Apc on Wnt Signaling in the Dorsal Telencephalon of Mus muscullis
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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 𝛽-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 𝛽-catenin levels in clumps of neural precursor-like cells. It was hypothesized that defunct Apc caused accumulation of 𝛽-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 𝛽-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 𝛽-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/+ 𝛽cat flox/flox hGFAP-Cre+ mutants presented similarly, suggesting a phenotype associated with 𝛽-catenin loss. Apc flox/+ 𝛽-cat flox/+ hGFAP-Cre + mutants appeared phenotypically normal. Apc flox/+ 𝛽-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 𝛽-catenin accumulation in the telencephalon, however the phenotype presented by 𝛽cat flox/flox hGFAP-Cre + mutants was of interest and will be studied in the future.