Identification of a Sgo2-Dependent but Mad2-Independent Pathway Controlling Anaphase Onset in Fission Yeast
| Autor: | Graham J. Buttrick, Liam J. Messin, Maria del Mar Mora-Santos, Kevin G. Hardwick, Jonathan B. A. Millar, Alicja M. Sochaj, John C. Meadows, Theresa C. Lancaster |
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| Rok vydání: | 2017 |
| Předmět: |
shugoshin
0301 basic medicine Mad1 Centromere BUB1 Glutamic Acid Cell Cycle Proteins Spindle Apparatus Cyclin B midzone Biology kinesin Article Anaphase-Promoting Complex-Cyclosome General Biochemistry Genetics and Molecular Biology 03 medical and health sciences 0302 clinical medicine Schizosaccharomyces Aurora Kinase B Kinetochores lcsh:QH301-705.5 Anaphase anaphase Lysine QH Cell Cycle Spindle midzone Nuclear Proteins fission yeast 3. Good health Cell biology Spindle checkpoint 030104 developmental biology lcsh:Biology (General) Securin Chromosome passenger complex spindle checkpoint Schizosaccharomyces pombe Proteins Asparagine Anaphase-promoting complex Mad2 030217 neurology & neurosurgery microtubule |
| Zdroj: | Cell Reports, Vol 18, Iss 6, Pp 1422-1433 (2017) Cell Reports |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2017.01.032 |
| Popis: | Summary The onset of anaphase is triggered by activation of the anaphase-promoting complex/cyclosome (APC/C) following silencing of the spindle assembly checkpoint (SAC). APC/C triggers ubiquitination of Securin and Cyclin B, which leads to loss of sister chromatid cohesion and inactivation of Cyclin B/Cdk1, respectively. This promotes relocalization of Aurora B kinase and other components of the chromosome passenger complex (CPC) from centromeres to the spindle midzone. In fission yeast, this is mediated by Clp1 phosphatase-dependent interaction of CPC with Klp9/MKLP2 (kinesin-6). When this interaction is disrupted, kinetochores bi-orient normally, but APC/C activation is delayed via a mechanism that requires Sgo2 and some (Bub1, Mph1/Mps1, and Mad3), but not all (Mad1 and Mad2), components of the SAC and the first, but not second, lysine, glutamic acid, glutamine (KEN) box in Mad3. These data indicate that interaction of CPC with Klp9 terminates a Sgo2-dependent, but Mad2-independent, APC/C-inhibitory pathway that is distinct from the canonical SAC. Graphical Abstract Highlights • Klp9 (kinesin-6) is required for re-localization of CPC to the spindle midzone • Klp9 plays a motor-independent role in controlling the timing of anaphase onset • Interaction of CPC and Klp9 terminates Sgo2-dependent inhibition of the APC/C • Mad3-Slp1 (Cdc20) is a bona fide inhibitor of APC/C in vivo Meadows et al. find that redistribution of the chromosome passenger complex (CPC) from centromeres to Klp9/MKLP2 at the spindle midzone terminates a Sgo2-dependent pathway controlling APC/C activation. Their data indicate that redistribution of CPC and Klp9 terminates a Mad2-independent, APC/C-inhibitory pathway that is distinct from the spindle assembly checkpoint. |
| Databáze: | OpenAIRE |
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