Figure 7. Homozygotes mutants of the genes glp-1 and skn-1 at 345 embryonic stage showed the abnormally formed tissue boundaries and the loss of tissue continuity required for normal early organogenesis. The mutation of the gene glp-1, a central regulator of the Notch signaling pathway, as shown in the cell population signaling network in Fig. 6, caused severe abnormalities in tissue boundary pattern formation and cell fate specification. The mutation of the gene skn-1, a downstream effector of the Notch signaling pathway, showed the abnormal development of pharynx, muscle and intestine characterized by the loss of tissue continuity and the abruptly formed tissue boundaries. The gene hm-2 and jac-1 gave rise to no significant phenotypes compared to the WT. The end-1 homozygotes mutants displayed the abnormalities in intestine development (Supplementary Fig. 8).