Mutations in the Plk gene lead to instability of Plk protein in human tumour cell lines

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Abstract
It has been established that mutations in Drosophila Polo cause abnormalities in mitosis1. 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, chromosome segregation and cytokinesis. Microinjection of anti-Plk antibody into living cells has been found to induce a mitotic abnormality that contributes to the generation of aneuploidy2, and this is an important finding in relation to tumour development. Indeed, previous studies have shown that the level of expression of a mitotic checkpoint gene, hsMAD2, is reduced3 and that another checkpoint gene, BUB1, is mutated in certain human cancer cells4.