Bulk RNA-Seq expression profiling of Defa6+ cells possessing either wild-type Tcf4 or homozygous loss of Tcf4 protein isolated from Apc-deficient colon tumor
T-cell factor 4 (Tcf4) protein (encoded by the Tcf7l2 gene) is a nuclear transcriptional regulator that plays a key role in the maintenance of intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 is an effector of the canonical Wnt signaling pathway. Aberrant activation of this pathway underlines the development and growth of intestinal tumors. The Apc-min (multiple intestinal neoplasia) mouse strain carries a single nucleotide mutation in one allele of the Apc tumor suppressor gene. Random deactivation of the second allele occurs during the life and results in the formation of multiple adenomas in the small intestine with occasional colonic occurence. The Defa6 promoter is active in adult small intestinal Paneth cells and its activation has been observed also in human colonic adenomas. To investigate the role of Tcf4 in Defa6+ colon adenoma cells, we used the Apc-min Rosa26-tdTomato Tcf7l2-wt/wt Defa6-iCre mouse strain. In this strain, cells with an active Defa6 promoter are marked by expression of a red fluorescent protein (tdTomato). At the same time, homozygous deletion of Tcf4 and Tcf4 protein was obtained in Tcf7l2-flox/flox litters, respectively. We performed gene expression profiling of Defa6-tdTomato+ cells isolated from mouse colon tumors.