期刊
DEVELOPMENTAL CELL
卷 16, 期 1, 页码 105-117出版社
CELL PRESS
DOI: 10.1016/j.devcel.2008.11.005
关键词
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资金
- NIGMS NIH HHS [R01 GM029513-28, R37 GM029513, R01 GM029513, GM29513] Funding Source: Medline
Premature anaphase onset is prevented by the mitotic checkpoint through production of a wait anaphase inhibitor(s) that blocks recognition of cyclin B and securin by Cdc20-activated APC/C, an E3 ubiquitin ligase that targets them for destruction. Using physiologically relevant levels of Mad2, Bub3, BubR1, and Cdc20, we demonstrate that unattached kinetochores on purified chromosomes catalytically generate a diffusible Cdc20 inhibitor or inhibit Cdc20 already bound to APC/C. Furthermore, the chromosome-produced inhibitor requires both recruitment of Mad2 by Mad1 that is stably bound at unattached kinetochores and dimerization-competent Mad2. We show that purified chromosomes promote BubR1 binding to APC/C-Cdc20 by acting directly on Mad2, but not BubR1. Our results support a model in which immobilized Mad1/Mad2 at kinetochores provides a template for initial assembly of Mad2 bound to Cdc20 that is then converted to a final mitotic checkpoint inhibitor with Cdc20 bound to BubR1.
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