Stuck in division or passing through: what happens when cells cannot satisfy the spindle assembly checkpoint.

  title={Stuck in division or passing through: what happens when cells cannot satisfy the spindle assembly checkpoint.},
  author={Conly L. Rieder and H{\'e}lder Maiato},
  journal={Developmental cell},
  volume={7 5},

The spindle-assembly checkpoint in space and time

Recent molecular analyses have begun to shed light on the complex interaction of the checkpoint proteins with kinetochores — structures that mediate the binding of spindle microtubules to chromosomes in mitosis.

Phosphatases: providing safe passage through mitotic exit

This work has shown that the key mitotic exit phosphatase in budding yeast, Cdc14, is now well understood, and in animal cells, it is now emerging that mitoticexit relies on distinct regulatory networks, including the protein phosphatases PP1 and PP2A.

Adapt or die: how eukaryotic cells respond to prolonged activation of the spindle assembly checkpoint.

Inhibition of factors involved in SAC adaptation could have important therapeutic applications by potentiating the ability of antimitotics to cause cell death.

Spindle Architectural Features Must Be Considered Along With Cell Size to Explain the Timing of Mitotic Checkpoint Silencing

The results suggest that spindle size does not always scale with cell size in mammalian cells and cell size is not sufficient to explain the differences in metaphase duration, and it is demonstrated that manipulating spindle geometry can alter mitotic and metaphaseduration.

Reconstituting the spindle assembly checkpoint and the signalling roles of Mad1

This study shows that Mad1 interacts with Bub1 in S. pombe to form a scaffold complex that is essential for SAC function, and provides evidence in support of the hypothesis that the C-terminus of Mad1 has additional roles in SAC signalling aside from Mad2 kinetochore recruitment.

Microtubules do not promote mitotic slippage when the spindle assembly checkpoint cannot be satisfied

Compared with cells lacking MTs, exit from mitosis is accelerated over a range of spindle poison concentrations that allow MT assembly because the SAC becomes satisfied on abnormal spindles and not because slippage is accelerated.

Sustaining the spindle assembly checkpoint to improve cancer therapy

It is found that the FCP1 phosphatase and its downstream target WEE1 kinase oppose the SAC, promoting mitosis exit despite malformed spindles, and it is shown that targeting this pathway might be useful for cancer therapy.

Mitosis and apoptosis: how is the balance set?




Mitotic forces control a cell-cycle checkpoint

This work applies tension to an improperly attached chromosome with a micromanipulation needle and finds that the entry into anaphase and the completion of mitosis was delayed by 5–6 hours when the misattached chromosome was placed under tension.

Attachment and tension in the spindle assembly checkpoint

This work has provided novel insights into the molecular mechanisms through which the spindle assembly checkpoint is regulated by both the attachment of chromosomes to kinetochore microtubules and the tension exerted on Kinetochores.

The spindle assembly checkpoint.

Survivin is required for a sustained spindle checkpoint arrest in response to lack of tension

It is shown that mammalian cells lacking survivin are unable to align their chromosomes, fail to recruit Aurora B to kinetochores and become polyploid at a very high frequency, demonstrating that survivin is not required for initial checkpoint activation, or for sustained checkpoint activation by loss of microtubules.

A cytokinesis checkpoint requiring the yeast homologue of an APC-binding protein

Checkpoint controls ensure that events of the cell-division cycle are completed with fidelity and in the correct order. In budding yeast with a mutation in the motor protein dynein, the mitotic

The checkpoint control for anaphase onset does not monitor excess numbers of spindle poles or bipolar spindle symmetry.

Analysis of the duration of mitosis in sea urchin zygotes and vertebrate somatic cells containing multipolar spindles found that animal cells do not have a checkpoint for the metaphase-anaphase transition that monitors defects in spindle architecture independent of the checkpoint that monitors kinetochore attachment to the spindle.

Aberrantly segregating centromeres activate the spindle assembly checkpoint in budding yeast

In all cases the division delays are completely abolished by the mad mutants that inactivate the spindle assembly checkpoint, demonstrating that the Mad gene products are required to detect the subtle defects in chromosome behavior that have been observed to arrest higher eukaryotic cells in mitosis.