Cell cycle regulators can be both maternal and/or zygotic. The knock out consortium recently provided the community with a deletion of a cyclin B homologue. This allele is located at genetic position 4.7 LG IV (ZC168.4), and we have found that it is required for postembryonic development. Previous studies from the van den Heuvel Lab showed that the maternal cyb homologue is required for early embryonic development. RNAi experiments showed that removing maternal product caused multiple nuclei, and the affected embryos arrested development at an early embryonic stage. Homozygous cyb mutants (
gk35 ) from heterozygous parents can survive embryogenesis, but show an early larval lethal phenotype. By injecting heterozygotes with a construct that contains a wild type copy of this cyb homologue, we found that most homozygous animals which contain both maternal product and the transgene grow up into sterile adults. Embryos from few fertile homozygous adults are either viable sterile animals or embryonic lethal which is consistent with the RNAi experimental results. All the viable animals expressed the co-transformation marker indicating the presence of the cyb -containing transgene. The possible explanation of these results is that maternal product of this cyb homologue allows the animal to go through embryogenesis, and the zygotic product is absolutely required for postembryonic development and sterility. Since transgenes can be expressed in the germline, albeit very inefficiently, few homozygous worms become fertile and give rise to the next generation. Transcriptional fusions of GFP showed that expression of the cyb homologue, which is very strong during embryogenesis, becomes weak after hatching and remains low throughout postembryonic development. At present, it is not clear whether the larval arrest phenotype is cell-cycle related, so we are presently engaged in determining the molecular and developmental basis of the early L1 arrest associated with cyb (
gk35) .