Abstract
In the fission yeast Schizosaccharomyces pombe, the septation initiation network (SIN) triggers cytokinesis after mitosis. We investigated the relationship between Dma1p, a spindle checkpoint protein and cytokinesis inhibitor, and the SIN. Deletion of dma1 inactivates the spindle checkpoint and allows precocious SIN activation, while overexpressing Dma1p reduces SIN signaling. Dma1p seems to function by inhibiting the SIN activator, Plo1p kinase, since dma1 overexpression and deletion phenotypes suggest that Dma1p antagonizes Plo1p localization. Furthermore, failure to maintain high cyclin-dependent kinase (CDK) activity during spindle checkpoint activation in dma1 deletion cells requires Plo1p. Dma1p itself localizes to spindle pole bodies through interaction with Sid4p. Our observations suggest that Dma1p functions to prevent mitotic exit and cytokinesis during spindle checkpoint arrest by inhibiting SIN signaling.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Cell Cycle Proteins / genetics*
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Cell Cycle Proteins / metabolism
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Cell Division / genetics
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Drosophila Proteins*
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Genes, cdc / physiology*
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Microtubule-Associated Proteins / genetics
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Microtubule-Associated Proteins / metabolism
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Microtubules / drug effects
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Microtubules / metabolism
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Mitosis / genetics*
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Models, Biological
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Mutation / genetics
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism
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Protein Structure, Tertiary / genetics
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Schizosaccharomyces / metabolism*
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Schizosaccharomyces pombe Proteins*
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Signal Transduction / genetics
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Spindle Apparatus / genetics*
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Spindle Apparatus / metabolism
Substances
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Cell Cycle Proteins
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Dma1 protein, S pombe
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Drosophila Proteins
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Microtubule-Associated Proteins
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Schizosaccharomyces pombe Proteins
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Sid4 protein, S pombe
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Protein Serine-Threonine Kinases