Mitotic arrest of mammalian cells significantly increases the vector 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 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 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
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
MASTL(Greatwall) regulates DNA damage responses by coordinating mitotic ... 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 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.
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
