Mechanism of cell slippage during mitotic arrest a Rapid degradation Biology Diagrams Whether recovery is a passive process in the absence of the checkpoint-inducing signals or requires active participation of specific effectors has not been explored extensively. A recent report 4 uncovers unsuspected roles of Cdk1 kinase in the recovery from SAC-induced mitotic arrest. This study in yeast shows that cells attempting to recover
Here, using a tunable system of chromosome mis-segregation, we show that mitotic errors trigger nuclear deformation, nuclear softening, and lamin and heterochromatin alterations, leading to rapid This is an important study on the damage-induced checkpoint maintenance and termination in budding yeast that provides novel and convincing evidence for a role of the spindle assembly checkpoint and mitotic exit network in halting the cell cycle after prolonged arrest in response to irreparable DNA double-strand breaks (DSBs). The study identifies particular components from these checkpoints
Mitotic arrest and cell fate: why and how mitotic inhibition of ... Biology Diagrams
Checkpoints are critical regulatory mechanisms within the eukaryotic cell cycle that ensure the accurate and timely progression of Screens for mutants that failed to arrest in mitosis after drug treatment led to the identification of six crucial proteins: Bub1, Bub2, Bub3 (collectively referred to as "budding uninhibited by benzimidazole
Recovery of TRF2 (TERF2) and other shelterin components by Flag-APEX2-TRF1 modestly decreased in abundance during mitotic arrest (Supplementary Fig. 1e), consistent with prior observations of Mitotic arrest elicits a localized caspase-dependent DNA damage response under the control of Bcl-2 family proteins. Cells were synchronized in prolonged mitosis for different times (N2M, N6M, N10M) and compared with untreated mitotic cells (M). We propose that recovery mechanisms also reduce caspase-3/7 activity to non-stressed levels
G1, G2, Metaphase (Spindle) Checkpoints Biology Diagrams
Here I discuss how the same mechanism--namely, inhibition of transcription during mitosis--can explain (1) apoptosis during mitotic arrest, (2) mitotic slippage, (3) G1 arrest after mitotic slippage and (4) secondary apoptosis after mitotic slippage. In fact, during mitotic arrest transcription is a โฆ
Polo-like kinase 1 (Plk1) is an important mitotic kinase that is crucial for entry into mitosis after recovery from DNA damage-induced cell cycle arrest. Plk1 activation is promoted by the conserved protein Bora (SPAT-1 in C. elegans), which stimulates the phosphorylation of a conserved residue in the activation loop by the Aurora A kinase.
