Mitotic arrest and apoptosis in response to epothilones Graphical Biology Diagrams 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 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 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.
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 The G2 DNA damage checkpoint is one of the most important mechanisms controlling G2-mitosis transition. mitotic entry after checkpoint recovery and APC/C activation in G2 arrest and 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
Cellular responses to a prolonged delay in mitosis are determined by a ... Biology Diagrams
A surveillance mechanism known as the mitotic checkpoint supervises the process of chromosome segregation and arrests cell cycle progression when the cells were treated with 3 ฮผg/ml ฮฑ-factor for 2 hours. To induce mitotic arrest, cells were treated with 15 ฮผg/ml of nocodazole (from a 100X stock in DMSO). In experiments with prolonged 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
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
