The distribution of mesendodermal cells was coordinated with the cell cycle through apoptosis, NF-κB, and Snail1a. In contrast to embryos injected with ConMO (A), distributions of the Casanova-expressing endodermal cells toward the animal pole were reduced in embryos injected with GemMO (B) or p21MO (I). Geminin mRNA (C), Cdt1MO (E), or MCM5MO (H) led to an appearance of Casanova-expressing cells at ectopic positions toward the animal pole, whereas Gem* mRNA was ineffective (D). (F) Casanova transcription was nearly lost in embryos overexpressing Cdt1. (G) Mutual rescue of the distribution of endodermal cells between GemMO and Cdt1MO were observed. (J) The appearance of Casanova-expressing cells at ectopic positions toward the animal pole caused by geminin mRNA was rescued by the coinjection of p53MO. (K) Snail1a (Sn1) mRNA rescued the reduced movements of Casanova-expressing cells toward the animal pole caused by GemMO. (L) Ectopic localization of Casanova-expressing cells caused by geminin mRNA was rescued by p65MO. The 60% epiboly embryos were viewed from the lateral with the dorsal to the right. (M–P) The cell cycle coordinates with formation of the ntl-expressing axial mesoderm. GemMO led to a posterior shift of the anterior boundary of ntl transcription, concommitant with a reduced body axis (N). In embryos injected with geminin mRNA, the anterior boundary of ntl was anteriorly shifted, and several ntl-expressing cells dispersed away from the midline notochord (O), which was rescued by the coinjection of p53MO (P). Arrowheads mark the anterior boundary of ntl transcription. The bud stage embryos were viewed from lateral with the dorsal to the right. The dorsal view of each embryo is shown in the bottom right corner. Bars, 100 µm.