Figure 6: A model of Kctd10 function in cardiogenesis.

In wild-type zebrafish embryos, the transcriptional activity of Tbx5 is moderated by Kctd10, and Tbx5 synergistically acts with other factors to restrict has2 at the prospective AVC region. When Kctd10 is deficient, Tbx5 is hyperactive to result in the ectopic expression of has2. Excess hyaluronic acid is deposited between myocardium and endocardium throughout the heart tube to lead to the malformations of AVC and heart looping failure.