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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Brown, Nicholas G. Haselbach, David Litos, Gabriele Brunner, Michael R. Imre, Richard Qiao, Renping Mechtler, Karl Stark, Holger Yamaguchi, Masaya Weissmann, Florian Peters, Jan-michael Jarvis, Marc A. Vanderlinden, Ryan Schulman, Brenda A. Davidson, Iain F. |
| Description | Author Affiliation: Qiao R ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Weissmann F ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Yamaguchi M ( Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105); Brown NG ( Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105); VanderLinden R ( Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105); Imre R ( Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna Biocenter (VBC), 1030 Vienna, Austria); Jarvis MA ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Brunner MR ( Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105); Davidson IF ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Litos G ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Haselbach D ( Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany); Mechtler K ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); Stark H ( Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany); Schulman BA ( Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105); Peters JM ( Research Institute of Molecular Pathology (IMP), Vienna Biocenter (VBC), 1030 Vienna, Austria); |
| Abstract | Chromosome segregation and mitotic exit are initiated by the 1.2-MDa ubiquitin ligase APC/C (anaphase-promoting complex/cyclosome) and its coactivator CDC20 (cell division cycle 20). To avoid chromosome missegregation, APC/C(CDC20) activation is tightly controlled. CDC20 only associates with APC/C in mitosis when APC/C has become phosphorylated and is further inhibited by a mitotic checkpoint complex until all chromosomes are bioriented on the spindle. APC/C contains 14 different types of subunits, most of which are phosphorylated in mitosis on multiple sites. However, it is unknown which of these phospho-sites enable APC/C(CDC20) activation and by which mechanism. Here we have identified 68 evolutionarily conserved mitotic phospho-sites on human APC/C bound to CDC20 and have used the biGBac technique to generate 47 APC/C mutants in which either all 68 sites or subsets of them were replaced by nonphosphorylatable or phospho-mimicking residues. The characterization of these complexes in substrate ubiquitination and degradation assays indicates that phosphorylation of an N-terminal loop region in APC1 is sufficient for binding and activation of APC/C by CDC20. Deletion of the N-terminal APC1 loop enables APC/C(CDC20) activation in the absence of mitotic phosphorylation or phospho-mimicking mutations. These results indicate that binding of CDC20 to APC/C is normally prevented by an autoinhibitory loop in APC1 and that its mitotic phosphorylation relieves this inhibition. The predicted location of the N-terminal APC1 loop implies that this loop controls interactions between the N-terminal domain of CDC20 and APC1 and APC8. These results reveal how APC/C phosphorylation enables CDC20 to bind and activate the APC/C in mitosis. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 19 |
| Volume Number | 113 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2016-05-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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