ArticleInternational journal of molecular sciences2014
Active transport can greatly enhance Cdc20:Mad2 formation.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- A minimal deterministic model reveals integration of spindle assembly and position checkpoints in mitosis.Scientific reports · 2025Article
- Trends in mathematical modeling of host-pathogen interactions.Cellular and molecular life sciences : CMLS · 2020Review
- Multi-scale stochastic organization-oriented coarse-graining exemplified on the human mitotic checkpoint.Scientific reports · 2019Article
- Systems Biology Modeling of Five Pathways for Regulation and Potent Inhibition of the Anaphase-Promoting Complex (APC/C): Pivotal Roles for MCC and BubR1.Omics : a journal of integrative biology · 2015Article
- Spindle assembly checkpoint is sufficient for complete Cdc20 sequestering in mitotic control.Computational and structural biotechnology journal · 2015Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To guarantee genomic integrity and viability, the cell must ensure proper distribution of the replicated chromosomes among the two daughter cells in mitosis.The mitotic spindle assembly checkpoint (SAC) is a central regulatory mechanism to achieve this goal. A dysfunction of this checkpoint may lead to aneuploidy and likely contributes to the development of cancer. Kinetochores of unattached or misaligned chromosomes are thought to generate a diffusible ''wait-anaphase'' signal, which is the basis for downstream events to inhibit the anaphase promoting complex/cyclosome (APC/C). The rate of Cdc20:C-Mad2 complex formation at the kinetochore is a key regulatory factor in the context of APC/C inhibition. Computer simulations of a quantitative SAC model show that the formation of Cdc20:C-Mad2 is too slow for checkpoint maintenance when cytosolic O-Mad2 has to encounter kinetochores by diffusion alone. Here, we show that an active transport of O-Mad2 towards the spindle mid-zone increases the efficiency of Mad2-activation. Our data indicate that this mechanism can greatly enhance the formation of Cdc20:Mad2 and furthermore gives an explanation on how the ''wait-anaphase'' signal can dissolve abruptly within a short time. Our results help to understand parts of the SAC mechanism that remain unclear.
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