Fig. 3. Loss-of-function in lin-23 triggers cell fate transformations and cdc-25.1-dependent hyperplasia. (A) DIC/GFP overlays of representative embryos expressing the intestinal-specific elt-2::gfp marker at 20°C. A wild-type embryo with 16 intestinal cells and a cdc-25.1(rr31) mutant with 30 intestinal cells are shown before morphogenesis. lin-23(e1883) null, lin-23(RNAi) and cdc-25.1(rr31); lin-23(RNAi) embryos at their terminal stages display obvious hyperplasia and lack morphogenetic movements. A cdc-25.1(rr31rr36) mutant treated with lin-23(RNAi) showing typical suppression of the lin-23-dependent intestinal hyperplasia. (B) Time lapse imaging of an embryo dissected from a lin-23(RNAi)-treated hermaphrodite undergoing Cp and MSp to E transformations. This embryo carries an integrated end-3::end-3(P202L)::gfp transgene that marks descendants of intestinal cells. Cells in the E, C- and MS-like lineages are highlighted. Double-headed arrows indicate the division axis of Ca- and Cp-like. Daughters of the normal E blastomere and those of two ectopic E-like cells are indicated by arrowheads as they begin to express the GFP marker. (C) Quantification of intestinal cell number in terminal stage lin-23(RNAi) and control embryos. The lin-23(RNAi)-dependent hyperplasia is not additive to cdc-25.1(gf), while penetrant and significant suppression (^*) of the cell cycle defects is seen when CDC-25.1 levels are reduced by rr36. E blastomeres (n=10) from lin-23(RNAi)-treated embryos (rightmost bar) were isolated by laser ablation as described by Zhu et al. (Zhu et al., 1997) and the number of intestinal cells, based on the expression of elt-2::gfp marker, was quantified 24 hours thereafter.