In early C. elegans embryos, cells are produced by asymmetric divisions and appear to be born with characteristic cell cycle times. For example, the first cleavage of the embryo produces a smaller posterior daugher blastomere called P1 that divides more slowly than the anterior daughter, called AB. These cell cycle differences may be important for proper regulation of pattern formation. To understand how these differences in cell cycle timing arise, and to determine if they are important for pattern formation, we have screened for mutants with alterations in the cell cycle timing of early embryonic cells. In a screen for temperature sensitive embryonic lethal mutants, we have identified three mutations,
or148,
or209 , and
or182 , that result in cell cycle delays in the early embryo. These three mutations define three separate genes based on genetic mapping and complementation tests. For one of these genes, defined by
or148 , we also have identified three non-conditional mutations that are allelic (
or16,
or17 , and
or27 ). A common phenotype of these mutants is a prolonged three cell stage due to a delay in the division of P1. In at least one of these mutants (
or182 , see abstract by Kathryn Swan), the delay of P1 is predominantly observed in this lineage. Preliminary observations of the terminal phenotype of these mutants suggest that these embryos frequently lack pharynx and intestine and instead make extra hypodermis. The two genes identified by alleles
or148 , and
or209 map to linkage group III. The position of
or148 is approximately at 2.0mu, just to the left of
unc-50 , and mapping of
or209 is underway. We are now microinjecting cosmids to obtain rescue of the mutant phenotype of
or148 . Cloning of these genes will give a more complete pictuire of their roles in cell division timing.