The nuclear division cycles of early Drosophila embryogenesis have a number of 
unique features that distinguish them from later cell cycles. These features 
include the lack of some checkpoints that operate in later cell cycles, the 
absence of gap phases, and very rapid DNA synthesis phases. The molecular 
mechanisms that control these rapid nuclear division cycles are poorly 
understood. Here we describe analysis of cyclin J, a previously uncharacterized 
cyclin which has an RNA expression pattern that suggests a possible role in 
early embryogenesis. We show that the cyclin J protein is present in early 
embryos where it forms active kinase complexes with cyclin-dependent kinase 
(Cdk) 2. To determine whether cyclin J plays a role in controlling the early 
nuclear cycles we isolated peptide aptamers that specifically bind to cyclin J 
and inhibit its ability to activate Cdks. We injected the inhibitory aptamers 
into syncytial Drosophila embryos and demonstrated that they caused defects in 
chromosome segregation and progression through mitosis. We obtained similar 
results by injecting cyclin J antibodies into embryos. Our results suggest that 
a cyclin J-associated kinase activity is required for the early embryonic 
division cycles.