Figure 1. The early lineage of the C. elegans embryo. Tissues produced by each of the founder cells (MS, E, C, D, P4) and by the four AB granddaughters are listed.

Figure 2. Localization of P granules (small black dots) and spindle orientations in wild-type and par mutants. (a) Distribution of P granules and PAR-1 and PAR-2 (blue) and PAR-3 and PAR-6 (red) proteins in the zygote. (b) Pattern after first cleavage and spindle orientations set up for the second cleavage. P granules are mislocalized in the mutant embryos.

Figure 3. Distribution of the SKN-1 (blue), PIE-1 (red), and PAL-1 (green) proteins in the first three cleavage stages. (a) Two-cell embryo: maternal SKN-1 protein is much higher in the P1 nucleus than in AB, and maternal PIE-1 protein is localized in P1. (b) Four-cell embryo: SKN-1 is high in both the P2 and EMS nuclei; PIE-1 is present in both the cytoplasm and nucleus of P2, and newly translated PAL-1 protein appears in the P2 and EMS nuclei. (c) Eight-cell embryo: SKN-1 is disappearing from all nuclei; PIE-1 is confined to the P3 nucleus; and PAL-1 is present in all four posterior nuclei although it functions only in C and D (see text).

Figure 4. Two signalling pathways set the AB and E blastomere fates by the 12-cell stage. (a) At the four-cell stage, P2 signals to AB.p through the APX-1–GLP-1 pathway, and also to EMS using the Wnt pathway. The localization of GLP-1 (green) and APX-1 (red) proteins is indicated. (b) Ventral view. At the 12-cell stage, MS signals to AB.alp and AB.ara, the two AB cells that contribute to the pharynx, to differentiate them from their sister cells, again through the GLP-1 pathway. The Wnt signal that polarizes EMS has inhibited POP-1 translation in E, with the result that intestinal-specific genes are activated there but inhibited by high POP-1 in MS. POP-1 blue; GLP-1, green; APX-1, red. Vertebrate and Drosophila homologues are listed in parentheses.