Abstract
In S. cerevisiae cells undergoing anaphase, a ras-related GTPase, Tem1, is located on the spindle pole body that enters the daughter cell and activates a signal transduction pathway, MEN, to allow mitotic exit. MEN activation must be reversed after mitotic exit to reset the cell cycle in G1. We find that daughter cells activate an Antagonist of MEN pathway (AMEN) in part through induction of the Amn1 protein that binds directly to Tem1 and prevents its association with its target kinase Cdc15. Failure of Amn1 function results in defects of both the spindle assembly and nuclear orientation checkpoints and delays turning off Cdc14 in G1. Thus, Amn1 is part of a daughter-specific switch that helps cells exit from mitotic exit and reset the cell cycle.
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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Binding Sites / genetics
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Cell Cycle / genetics*
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism*
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Cells, Cultured
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Eukaryotic Cells / cytology
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Eukaryotic Cells / metabolism*
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GTP-Binding Proteins / genetics
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GTP-Binding Proteins / metabolism*
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Genes, cdc / physiology*
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Mitosis / genetics
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Molecular Structure
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Protein Binding / genetics
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RNA-Binding Proteins
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Saccharomyces cerevisiae
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / metabolism*
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Signal Transduction / genetics*
Substances
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Amn1 protein, S cerevisiae
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CDC15 protein
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CEF1 protein, S cerevisiae
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Cell Cycle Proteins
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RNA-Binding Proteins
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Saccharomyces cerevisiae Proteins
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GTP-Binding Proteins