Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the yeast Saccharomyces cerevisiae.
Inhibition of mitosis by antimitotic drugs is thought to occur by destruction of microtubules, causing cells to arrest through the action of one or more mitotic checkpoints. We have patterned experiments in the yeast Saccharomyces cerevisiae after recent studies in mammalian cells that demonstrate the effectiveness of antimitotic drugs at concentrations that maintain spindle structure. We show that low concentrations of nocodazole delay cell division under the control of the previously identified mitotic checkpoint genes BUB1, BUB3, MAD1, and MAD2 and independently of BUB2. The same genes mediate the cell cycle delay induced in ctf13 mutants, limited for an essential kinetochore component. Our data suggest that a low concentration of nocodazole induces a cell cycle delay through checkpoint control that is sensitive to impaired kinetochore function. The BUB2 gene may be part of a separate checkpoint that responds to abnormal spindle structure.
Department of Biology, University of Virginia, Charlottesville 22903, USA.
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Y
Wang
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Burke
D002455:Cell Division / Q000187:drug effects / Q000235:genetics; D005800:Genes, Fungal / Q000187:drug effects / Q000502:physiology*; D005838:Genotype; D007700:Kinetics; D018386:Kinetochores / Q000187:drug effects / Q000502:physiology*; D008870:Microtubules / Q000187:drug effects / Q000502:physiology; D008938:Mitosis / Q000187:drug effects; D009154:Mutation; D015739:Nocodazole / Q000494:pharmacology*; D012441:Saccharomyces cerevisiae / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D014404:Tubulin / Q000032:analysis
D014404:Tubulin; D015739:Nocodazole