High impact information on tcf7l1a

• Here we describe the zebrafish headless (hdl) mutant and show that its severe head defects are due to a mutation in T-cell factor-3 (Tcf3), a member of the Tcf/Lef family [1].
• Systematic changes in gene expression caused by reduced Tcf3 function help predict the shape of a caudalizing activity gradient that defines compartments along the rostral-caudal axis [2].
• In zebrafish, basal repression of caudal genes is achieved through the function of Headless (Hdl), a Tcf3 homolog [2].
• Loss of Lef1 activity results in decreased reporter expression and posterior defects, while loss of Tcf3 (Headless, Hdl) activity does not alter reporter expression, even though it results in loss of forebrain structures [3].
• Overexpression of mutant zTcf-3 products and Cadherin leads to a reduction in the expression of the dorsal-specific genes goosecoid and chording at the blastula stages, indicating a conserved role for betacat and tcf-3 in zebrafish dorsal axis induction [4].

Analytical, diagnostic and therapeutic context of tcf7l1a

• We report the molecular cloning and expression of the zebrafish tcf-3 homologue and study its function and that of zebrafish betacat in dorsoventral patterning [4].

References