The role of Pph3 in checkpoint recovery is at least in part due to its function as a γH2AX phosphatase, as the delay in checkpoint recovery manifested by pph3Δ cells is largely alleviated by the expression of a non-phosphorylatable H2A mutant (Keogh et al, 2006).
Disturbance of CPC function results in chromosome congression and segregation defects due to stabilization of incorrect kinetochore microtubule attachments, an impaired function of the mitotic checkpoint and improper spindle formation.
Some cancer cells with weakened spindle checkpoint function were reported to show elevated sensitivity to microtubule inhibitors (13).
Nocodazole treatment presumably causes maximal mitotic checkpoint signaling due to the fact that all kinetochores are unattached.
The above experiments have analyzed markers of the checkpoint and have suggested that Cdc14 is required to prevent checkpoint reengagement due to loss of tension at anaphase onset.
This demonstrates that Cdc14 can override a mitotic checkpoint delay due to absence of tension between sister chromatids.
They had sex, but he was unable to function properly due to recent prostate surgery.
Possibly, these chromosomes are unattached but fail to activate the mitotic checkpoint due to diminished Mps1 activity.
The majority of tumors are deficient in the G1/S DNA damage checkpoint due to tumor suppressor p53 mutations.
In fact, sen1 mutants generate checkpoint signals, likely due to fork pausing and/or DNA-RNA hybrid processing.
