The complex process of embryogenesis in the simple nematode Caenorhabditis elegans is invariant from animal to animal. Cell lineages have been studied by direct observation of individual cells in living embryos using Nomarski differential-interference-contrast microscopy. To dissect events genetically involved in embryogenesis, we have isolated a set of 36 recessive temperature-sensitive (ts) mutants in 30 separate emb-genes, which cause arrest of embryonic development. The fraction of emb mutants among total ts lethals and the recurrence frequency (second alleles) allowed two independent estimates of 200-500 genes essential for embryogenesis (of a total of about 2000 essential genes). So far 54 emb genes have been detected, still far from genetic saturation. We have mapped 25 new emb genes (resolution of 1 recombination unit). Surprisingly, 10 emb genes are clustered near gene
unc-32 on linkage group III. Higher resolution mapping here, using deletions, is under way. We have tested the mode of expression (the necessity and/or sufficiency for normal embryogenesis) of the wild-type alleles of these 30 genes in the parents and zygote by performing genetic crosses in which a wild-type allele appears in various configurations, and then determining at the restrictive temperature (25C) the effect on the viability of the resulting progeny genotypes. A majority of the emb genes are of maternal-expression-necessary class (18 of 30 genes studied), in agreement with the results from other similar mutants. For 3 genes, neither maternal nor zygotic expression is sufficient (both necessary?). We have also found 2 zygotic-necessary-and-sufficient genes. For 1 gene paternal expression is partially sufficient. The remaining 7 are of the parental-or-zygotic-expression-sufficient class. We have ordered the ts mutants sequentially in development by temperature shift experiments and according to their arrest stage (terminal phenotypes). Their cellular and subcellular properties are being studied to identify the cellular processes defective in the mutants, and ultimately the mechanisms for genetic control of cell behavior in embryogenesis. We are finding a variety of defects in early cell lineages, including the timing of embryonic cell divisions similar to those already described in another set of mutants.