Inefficient degradation of cyclin B1 re-activates the spindle checkpoint right after sister chromatid disjunction

Puerarin Exerts a Delayed Inhibitory Effect on the Proliferation of Cardiomyocytes Derived from Murine ES Cells via Slowing Progression through G2/M Phase

“…It has been confirmed that the Cyclin A2-Cdk1 complex triggers Cyclin B1-Cdk1 activation [31], which causes break down of nuclear envelope to allow mitotic spindle to access the chromosomes [32]. At anaphase, highly active anaphasepromoting complexes support the degradation of Cyclin B1-Cdk1 complex and thereby inactivate the Cdk1 which initiates mitotic exit and reestablishment of the interphase state [30,33]. Our study shows that the transcription levels of Cyclin A2, Cyclin B1 and Cdk1 are increased in puerarin treated ES-CMs.…”

“…The amount of cyclin B and the activity of the Cyclin B-Cdk1 complex rise through the cell cycle until mitosis. After anaphase, they fall suddenly due to degradation of cyclin B [30]. In the cell cycle phases, Cyclin A2 binds Cdk1 during the transition from G2 to M phase.…”

Nek2A destruction marks APC/C activation at the prophase-to-prometaphase transition by spindle-checkpoint restricted Cdc20

“…Likely, checkpoint silencing will not only permit increased UbcH10 binding, but also increased Ube2S binding and thus higher APC/C catalytic activity . Recently, we and others proposed that enhanced APC/C Cdc20 activity upon spindle checkpoint release might help to avoid the 'anaphase problem': the risk that separating sister chromatids when losing tension could re-impose the spindle checkpoint in case cyclin B1 is not completely degraded when cells reach anaphase (Clijsters et al, 2014;Kamenz and Hauf, 2014;Rattani et al, 2014;Vázquez-Novelle et al, 2014). The implications of these findings require further analysis of the way changes in APC/C Cdc20 influence mitotic exit.…”

The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation

“…The results showed that even a modest amount of residual cyclin B in anaphase can trigger SAC reactivation, in turn, stabilizing any leftover cyclin B and shutting down mitotic progression. 66 Clearly, mitotic cells must guarantee thorough and timely cyclin B clearance to irreversibly shut down SAC, a task that may be ensured by actively concentrating cytoplasmic cyclin B to the centrosomes just prior to the initiation of degradation. Probing the mechanisms by which cyclin B is targeted to the centrosome would allow further studies to test the functional relevance of cyclin B centrosomal enrichment on Figure 2.…”