Figure 2. β-catenin-driven binary cell fate switches in the ascidian embryo.

(A) Two β-catenin switches in wild-type embryos after animal-vegetal oriented cell divisions. The scheme depicts one of the two sister cell pairs a4.2 and A4.1 from an 8-cell stage ascidian embryo, and its progeny (anterior views, animal pole to the top, vegetal pole to the bottom). The animal-pole sister a4.2 and its descendants exhibit only low levels of nuclear β-catenin protein, and will adopt ectodermal cell fates. The vegetal-pole sister A4.1, and its descendants A5.1 and A5.2 exhibit high levels of nuclear β-catenin adopting endomesodermal cell fate. Both, A5.1 and A5.2 divide to form animal-pole sisters with low β-catenin levels adopting margin cell fate (mesoderm and ectoderm), and vegetal-pole sisters with high β-catenin levels adopting endodermal cell fates. (B) Ectopic β-catenin switches specify endoderm versus margin cell fate in the ectodermal cell lineage a4.2. Ectopically elevating β-catenin levels in the animal pole sister a4.2 causes a4.2 to adopt the endomesodermal cell fate of its vegetal pole sister A4.1, and the subsequent formation of an ectopic A5.1* and A5.2* daughter cell pair. Ectopic inhibition of β-catenin in A5.1* causes its sister cell pair to adopt margin cell fate, whereas high levels of β-catenin in A5.2* promote endodermal cell fate. High and low nuclear levels of β-catenin protein are indicated (red nucleus: βcat high; white nucleus: βcat low). Sister cells are connected by black bars. Adopted cell fates are shown in boxes, and grey scale-coded accordingly in sister cells.