We are interested in the molecular mechanisms by which embryonic cells stop dividing and assume particular differentiated fates, and are studying this problem in a model system, the nematode C. elegans. This work will continue to complement genetic and molecular work on the other intensely studied invertebrate, Drosophila. These studies will thus provide a broader picture of animal development and shed light on both concepts and mechanisms of development in higher animals. To identify molecules that control cell fate in C. elegans, animal are mutagenized and screened for the appearance of mutants that lack, or overproduce, specific cell types. The phenotypes of these mutants are then analyzed to determine the development basis for the defect. mutants that appear defective in specifying cell fate, as opposed to being defective in general cell differentiation, are selected for further genetic and molecular analysis. The work proposed in this grant focuses on how certain early embryonic cells in C. elegans choose to become muscle cells. We have identified one class of mutants in which an early embryonic cell that normally does not produce muscles inappropriately produces numerous muscles. In a second class of mutants, a different early embryonic cell that normally produces numerous muscles instead produces intestinal cells. Genetic and molecular analysis of these mutants should provide clues to how embryonic cells in normal embryos make choices between muscle and non-muscle fates.
