Some transforming oncogenes directly abrogate spindle checkpoint function, which presumably results in genomic instability. Checkpoint genes from yeast to humans are have been identified on the basis of conserved sequences suggesting that there are fundamental aspects of the checkpoint mechanism shared by all cells. Experimental evidence collected by us and others show that the functions of the conserved genes are very similar to those in yeast. This suggests that there is a similar mechanism of inducing a mitotic arrest, when the checkpoint is activated. It is important to understand how this checkpoint arrest is mediated because several chemotherapeutic drugs, such as taxol induce a mitotic arrest that is checkpoint dependent.
Human cells respond to a prolonged mitotic arrest by inducing apoptosis.
The lessons should be directly applicable to similar studies in human cells. Reference List Kallio, M., J. Weinstein, J.R. Daum, D.J. Burke, and G.J. Gorbsky. Cell cycle arrest in cdc20 mutants of Saccharomyces cerevisiae is independent of Ndc10p and kinetochore function but requires a subset of spindle checkpoint genes. Differential requirements for DNA replication in the activation of mitotic checkpoints in Saccharomyces cerevisiae. Wang, Y. and D.J. Burke.