INTRODUCTION Thirteen cycles of rapidly alternating DNA synthesis and nuclear division follow the fertilisation of a Drosophila melanogaster egg. These cycles are unusual in at least two

Thirteen cycles of rapidly alternating DNA synthesis and nuclear division follow the fertilisation of a Drosophila melanogaster egg. These cycles are unusual in at least two ways. Firstly, the syncytial division cycles lack the checkpoint that prevents entry into mitosis in the presence of unreplicated DNA. Thus injection of aphidicolin into embryos prevents DNA replication but has little effect on mitosis, with both centrosome replication and nuclear envelope breakdown cycles proceeding normally (Raff and Glover, 1988). Secondly, the mitotic Aand B-type cyclins do not undergo complete degradation at the metaphaseanaphase transition in the rapid division cycles (Maldonado-Codina and Glover, 1992). After nuclear division 7 the majority of nuclei begin to migrate towards the periphery of the embryo, although some remain in the interior, cease dividing and become the polyploid yolk nuclei. The dividing nuclei have approached the surface by the time of the tenth nuclear division and form a monolayer just beneath it. During migration and in the syncytial blastoderm stages, when the nuclei are at the cortex, the time taken for each cell cycle increases, from 9 minutes for cycle 8 to 21 minutes for cycle 13 (Foe and Alberts, 1983). If any of divisions 11 to 13 at the embryo periphery are aberrant the affected nuclei may sink towards the central part of the embryo (Sullivan et al., 1990). This loss of nuclei from the surface monolayer appears to be a generalised reaction to defective chromosome segregation (Minden et al., 1989; Warn et al., 1987). A small subset of nuclei become cellularised immediately upon reaching the posterior pole to form the pole cells, precursors of the adult germline. These cells no longer divide synchronously with the syncytial nuclei. Cellularisation of the remaining nuclei takes place in the interphase of cycle 14 following four further divisions at the cortex. Maternally provided gene products are sufficient to drive the syncytial cycles (Szabad and Bryant, 1982). Mutations in these maternally expressed genes can give rise to mitotic defects in early embryos. Some of these genes, for example giant nuclei (gnu) (Freeman et al., 1986; Freeman and Glover, 1987), encode proteins that are apparently only required in the syncytial embryo. Females homozygous for mutations at the gnu locus produce eggs that undergo multiple rounds of DNA replication without any nuclear division. Centrosome replication occurs independently of the formation of these giant nuclei (Freeman et al., 1986; Freeman and Glover, 1987). Maternal effect mutations in other genes, plutonium and pan gu, have also been described to have similar phenotypes (Shamanski and Orr-Weaver, 1991). The autonomous replication of centrosomes appears to be a general consequence of disrupting mitosis in syn87 Journal of Cell Science 106, 87-98 (1993) Printed in Great Britain © The Company of Biologists Limited 1993