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. 2014 Aug 27;9(8):e105886. doi: 10.1371/journal.pone.0105886

Figure 1. Schematic representation of genetic engineering of the β-Catenin-driven chimeric colon model.

Figure 1

A). In ES cells: 3 transgenic cassettes were inserted: Villin-Cre, GAPDH-lox-stop-lox-rtTA-IRES-Luciferase, and TetO- β-CateninΔN131; all three remain silent in ES cells. In addition, one p53 allele was floxed and expresses wild type p53 in ES cells and the other allele was targeted with lox-stop-lox and R172H point mutation, which is functionally null in ES cells. B). In the gastro-intestinal epithelium, expression of Cre leads to deletion of the two lox-stop-lox cassettes as well as the floxed p53 allele. p53 expression will switch from wild type to the mutant form, and expression of rtTA and Luciferase will switch on. C). in the presence of doxycycline, rtTA will bind to the TetO promoter and activate transcription of β-CateninΔN131.