Two adjacent cells in the nematode worm normally differentiate into an anchor cell (AC) and a ventral uterine precursor (VU) cell, but which of the two becomes the AC and which becomes the VU cell is completely random: the cells have an equal chance of adopting either fate, but they always adopt different fates. Mutations of Lin12 alter these fates. In hyperactive Lin12 mutants, both cells become VU cells, while in inactive Lin12 mutants, both cells become ACs. Thus, Lin12 is central to the decision making process. In genetic mosaics in which one precursor cell has the hyperactive Lin12 and the other precursor has the inactive Lin12, the cell with the hyperactive Lin12 always becomes the VU cell and the cell with inactive Lin12 always becomes the AC. Assuming that one cell sends a signal and the other cell receives it, explain how these results suggest that Lin12 encodes a protein required to receive the signal. Offer a suggestion for how the fates of these two precursor cells are normally decided in wildtype worms.