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T‐cell factor 4 (Tcf7l2) maintains proliferative compartments in zebrafish intestine
Author(s) -
Muncan Vanesa,
Faro Ana,
Haramis AnnaPavlina G,
Hurlstone Adam F L,
Wienholds Erno,
van Es Johan,
Korving Jeroen,
Begthel Harry,
Zivkovic Danica,
Clevers Hans
Publication year - 2007
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7401071
Subject(s) - biology , zebrafish , microbiology and biotechnology , mesenchyme , wnt signaling pathway , tcf4 , intestinal epithelium , epithelium , stomach , genetics , embryo , transcription factor , signal transduction , gene , biochemistry , enhancer
Previous studies have shown that Wnt signals, relayed through β‐catenin and T‐cell factor 4 (Tcf4), are essential for the induction and maintenance of crypts in mice. We have now generated a tcf4 ( tcf7l2 ) mutant zebrafish by reverse genetics. We first observe a phenotypic defect at 4 weeks post‐fertilization (wpf), leading to death at about 6 wpf. The phenotype comprises a loss of proliferation at the base of the intestinal folds of the middle and distal parts of the intestine. The proximal intestine represents an independent compartment, as it expresses sox2 in the epithelium and barx1 in the surrounding mesenchyme, which are early stomach markers in higher vertebrates. Zebrafish are functionally stomach‐less, but the proximal intestine might share its ontogeny with the mammalian stomach. Rare adult homozygous tcf4 −/− ‘escapers’ show proliferation defects in the gut epithelium, but have no other obvious abnormalities. This study underscores the involvement of Tcf4 in maintaining proliferative self‐renewal in the intestine throughout life.