Embryonic, somatic and germ cell divisions are tightly controlled both temporally and spatially. The mechanisms that control these divisions are complex, but appear to use the same conserved regulators found in other organisms. For example, the cyclin-dependent kinase CDC-2 controls the entry into M-phase. Investigations into how CDC-2 is regulated may show how the different cell cycles are established and maintained. CDC2 is activated by a dual specificity phosphatase called CDC25. Whereas other organisms are known to have between one and three
cdc25 genes, four
cdc25 homologues have been identified in the C. elegans genome (called
cdc-25.1 ,
cdc-25.2 ,
cdc-25.3 and
cdc-25.4 ). Interestingly, only the first three homologues appear to be expressed in wild-type hermaphrodites.
cdc-25.2 has two transcripts. Both transcripts have the phosphatase domain while only the larger transcript has the putative regulation domain. Only the longer transcript is expressed in embryos, whereas the shorter transcript is present in adults. Perturbation of
cdc-25.2 by RNAi causes L1 larval lethality. However, if all three
cdc-25s that are expressed are perturbed at the same time, the cell cycle is arrested during the first meiotic division. The mutant
emb-29 maps very close to the
cdc-25.2 locus. Indeed, two
emb-29 alleles at the restrictive temperature produce cell cycle phenotypes -
emb-29 mutants arrest at the G2/M transition [1]. Furthermore, simultaneous RNAi of
cdc-25.1 and
cdc-25.3 in either
emb-29 background causes a meiotic arrest similar to the triple
cdc-25 RNAi phenotype. Unfortunately, only one
emb-29 allele harbours a point mutation in the
cdc-25.2 gene. We are determining whether this point mutation alters the activity of the CDC-25.2 protein. Nevertheless, we suspect that
emb-29 (+) may regulate CDC-25.2: any defect in
emb-29 may effect the activity of CDC-25.2 thus causing a cell cycle phenotype. 1. Hecht et al. (1987) J. Cell Science 87, 305-314.