Abstract
In Saccharomyces cerevisiae and HeLa cells, the NoCut checkpoint, which involves the chromosome passenger kinase Aurora B, delays the completion of cytokinesis in response to anaphase defects. However, how NoCut monitors anaphase progression has not been clear. Here, we show that retention of chromatin in the plane of cleavage is sufficient to trigger NoCut, provided that Aurora/Ipl1 localizes properly to the spindle midzone, and that the ADA histone acetyltransferase complex is intact. Furthermore, forcing Aurora onto chromatin was sufficient to activate NoCut independently of anaphase defects. These findings provide the first evidence that NoCut is triggered by the interaction of acetylated chromatin with the passenger complex at the spindle midzone.
Publication types
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Letter
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Research Support, Non-U.S. Gov't
MeSH terms
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Aurora Kinases
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Cell Cycle Proteins / metabolism
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Chromosomal Proteins, Non-Histone / metabolism
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Chromosome Segregation*
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Cytokinesis
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Endopeptidases / metabolism
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Histone Acetyltransferases / metabolism
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Intracellular Signaling Peptides and Proteins
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Microtubules / metabolism
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Protein Binding
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Protein Kinases / metabolism
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Protein Serine-Threonine Kinases / metabolism*
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Protein Transport
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Saccharomyces cerevisiae / cytology
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Saccharomyces cerevisiae / enzymology
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Saccharomyces cerevisiae / metabolism*
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Saccharomyces cerevisiae Proteins / metabolism*
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Separase
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Spindle Apparatus / metabolism
Substances
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AHC1 protein, S cerevisiae
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Cell Cycle Proteins
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Chromosomal Proteins, Non-Histone
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Intracellular Signaling Peptides and Proteins
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Saccharomyces cerevisiae Proteins
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Histone Acetyltransferases
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Protein Kinases
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Aurora Kinases
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IPL1 protein, S cerevisiae
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Protein Serine-Threonine Kinases
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Endopeptidases
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Separase