It has been established that mutations in Drosophila Polo cause abnormaliti
es in mitosis(1). In human cells, maximal Plk activity is reached in the M
phase of the cell cycle, and the function of Plk is therefore considered to
be required for mitotic cellular events such as spindle formation, chromos
ome segregation and cytokinesis. Microinjection of antiPlk antibody into li
ving cells has been found to induce a mitotic abnormality that contributes
to the generation of aneuploidy(2), and this is an important finding in rel
ation to tumour development. Indeed, previous studies have shown that the l
evel of expression of a mitotic checkpoint gene, hsMAD2, is reduced(3) and
that another checkpoint gene, BUB1, is mutated in certain human cancer cell
s(4).