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In yeast, anaphase entry depends on Pds1 proteolysis, while chromosome re-duplication in the subsequent S-phase involves degradation of mitotic cyclins such as Clb2. Sequential proteolysis of Pds1 and mitotic cyclins is mediated by the anaphase-promoting complex (APC). Lagging chromosomes or spindle damage are detected by surveillance mechanisms (checkpoints) which block anaphase onset, cytokinesis and DNA re-replication. Until now, the MAD and BUB genes implicated in this regulation were thought to function in a single pathway that blocks APC activity. We show that spindle damage blocks sister chromatid separation solely by inhibiting APCCdc20-dependent Pds1 proteolysis and that this process requires Mad2. Blocking APCCdh1-mediated Clb2 proteolysis and chromosome re-duplication does not require Mad2 but a different protein, Bub2. Our data imply that Mad1, Mad2, Mad3 and Bub1 regulate APCCdc20, whereas Bub2 regulates APCCdh1.

Original publication

DOI

10.1093/emboj/18.10.2707

Type

Journal article

Journal

EMBO J

Publication Date

17/05/1999

Volume

18

Pages

2707 - 2721

Keywords

Anaphase, Anaphase-Promoting Complex-Cyclosome, Calcium-Binding Proteins, Carrier Proteins, Cell Cycle, Cell Cycle Proteins, Chromosomal Proteins, Non-Histone, Cyclin B, Cyclins, DNA Replication, Fungal Proteins, GTP-Binding Proteins, Interphase, Ligases, Mad2 Proteins, Mitosis, Monomeric GTP-Binding Proteins, Mutation, Nocodazole, Nuclear Proteins, Phosphoproteins, Repressor Proteins, Saccharomyces cerevisiae Proteins, Schizosaccharomyces pombe Proteins, Securin, Sister Chromatid Exchange, Spindle Apparatus, Ubiquitin-Protein Ligase Complexes, Ubiquitin-Protein Ligases, Yeasts