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Fig. 2. Stabilization of CDC-25.1 triggers intestinal hyperplasia during a specific developmental window. The wild-type intestinal lineage is shown on the left with its typical division timing in minutes after pronuclear meeting at 20°C. The end-3 gene is transcribed during the E¹ and E² stages (black bar) (Maduro et al., 2007), while GFP alone expressed from the end-3 promoter is visible from E² to threefold stage (550 minutes) (green bar). DIC/GFP overlays of wild-type transgenic embryos expressing the indicated GFP::CDC-25.1 fusion protein variants under the control of the end-3 promoter. The average time in minutes at which the degradation was complete is shown beneath each column. Degradation of the GFP::CDC-25.1[WT] fusion protein occurs 20 minutes after the E^4-8 cell division. GFP::CDC-25.1[G47D] resists degradation for more than 120 minutes and triggers a supernumerary division 40-45 minutes into the E⁸-cell stage, resulting in a precocious E¹⁶-like stage and an abnormal hyperplasic E³²-cell stage. The intragenic mutation restores proper degradation of GFP::CDC-25.1[G47D;L273F] with kinetics similar to the wild type, while GFP::CDC-25.1[L273F] is destabilized prematurely. Stabilization and hyperplasia typical of GFP::CDC-25.1[G47D] protein are detected in lin-23(RNAi)-treated animals expressing GFP::CDC-25.1[WT], while the [L273F] substitution suppresses these phenotypes. These lin-23(RNAi) embryos do not undergo cell fate transformation (see text). Exposure time was increased to similar levels in all 220 and 260 minute embryos. All embryos were assayed at 20°C. In the last two columns, these embryos were classified based on their intestinal cell stage, owing to the effect of lin-23(RNAi) treatment on the E division timing (Z. Bao, personal communication).

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