Positive feedback promotes mitotic exit via the APC/C-Cdh1-separase-Cdc14 axis in budding yeast

The mitotic inhibitor securin is degraded via the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C)-Cdc20 after anaphase onset. This triggers activation of the mitotic protease separase and thereby sister chromatid separation. However, only a proportion of securin molecules are degraded...

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Bibliographic Details
Published in:Cellular signalling 2016-10, Vol.28 (10), p.1545-1554
Main Authors: Hatano, Yuhki, Naoki, Koike, Suzuki, Asuka, Ushimaru, Takashi
Format: Article
Language:English
Subjects:
Anaphase-Promoting Complex-Cyclosome - metabolism
Feedback, Physiological
Mitosis
Models, Biological
Protein Binding
Proteolysis
Saccharomyces cerevisiae
Saccharomyces cerevisiae Proteins - metabolism
Saccharomycetales - cytology
Saccharomycetales - metabolism
Securin - metabolism
Separase - metabolism
Signal Transduction
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Summary:The mitotic inhibitor securin is degraded via the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C)-Cdc20 after anaphase onset. This triggers activation of the mitotic protease separase and thereby sister chromatid separation. However, only a proportion of securin molecules are degraded at metaphase-anaphase transition and the remaining molecules are still present in anaphase. The roles of securin and separase in late mitosis remain elusive. Here, we show that securin still inhibits separase to repress mitotic exit in anaphase in budding yeast. APC/C-Cdh1-mediated securin degradation at telophase further liberated separase, which promotes Cdc14 release and mitotic exit. Separase executed these events via its proteolytic action and that in the Cdc14 early release (FEAR) network. Cdc14 release further activated APC/C-Cdh1 in the manner of a positive feedback loop. Thus, the positive feedback promotes mitotic exit via the APC/C-Cdh1-separase-Cdc14 axis. This study shows the importance of the two-step degradation mode of securin and the role of separase in mitotic exit.
ISSN:0898-6568
1873-3913
DOI:10.1016/j.cellsig.2016.07.005