ArticleThe Journal of biological chemistry2008
The spindle checkpoint functions of Mad3 and Mad2 depend on a Mad3 KEN box-mediated interaction with Cdc20-anaphase-promoting complex (APC/C).
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 107 citations in OpenAlex.
- BubR1 TPR domain supports the mitotic checkpoint by promoting MCC formation and MCC-APC/C interaction.Communications biology · 2026Article
- Autophagy-related protein Atg11 is essential for microtubule-mediated chromosome segregation.PLoS biology · 2025Article
- Article
- MAPK-dependent control of mitotic progression in S. pombe.BMC biology · 2024Article
- Kinetochore-catalyzed MCC formation: A structural perspective.IUBMB life · 2023Article
- Recovery from spindle checkpoint-mediated arrest requires a novel Dnt1-dependent APC/C activation mechanism.PLoS genetics · 2022Article
- Mitotic checkpoint gene expression is tuned by codon usage bias.The EMBO journal · 2022Article
- Biochemical, biophysical, and functional characterisation of the E3 ubiquitin ligase APC/C regulator CDC20 fromFrontiers in physiology · 2022Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Mechanisms for the temporal regulation of substrate ubiquitination by the anaphase-promoting complex/cyclosome.Cell division · 2019Review
- Implications of alternative routes to APC/C inhibition by the mitotic checkpoint complex.PLoS computational biology · 2018Article
- BubR1 Promotes Bub3-Dependent APC/C Inhibition during Spindle Assembly Checkpoint Signaling.Current biology : CB · 2017Article
- Identification of a Sgo2-Dependent but Mad2-Independent Pathway Controlling Anaphase Onset in Fission Yeast.Cell reports · 2017Article
- Taming the Beast: Control of APC/CCold Spring Harbor symposia on quantitative biology · 2017Article
- A novel mutation in the N-terminal domain of Drosophila BubR1 affects the spindle assembly checkpoint function of BubR1.Biology open · 2016Article
- Prognostic implications of securin expression and sub-cellular localization in human breast cancer.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- Mps1Mph1 Kinase Phosphorylates Mad3 to Inhibit Cdc20Slp1-APC/C and Maintain Spindle Checkpoint Arrests.PLoS genetics · 2016Article
- The mitotic checkpoint complex (MCC): looking back and forth after 15 years.AIMS molecular science · 2016Article
- Bub3-BubR1-dependent sequestration of Cdc20Fizzy at DNA breaks facilitates the correct segregation of broken chromosomes.The Journal of cell biology · 2015Article
- Understanding the structural basis for controlling chromosome division.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2015Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Mitotic progression is driven by proteolytic destruction of securin and cyclins. These proteins are labeled for destruction by an ubiquitin-protein isopeptide ligase (E3) known as the anaphase-promoting complex or cyclosome (APC/C). The APC/C requires activators (Cdc20 or Cdh1) to efficiently recognize its substrates, which are specified by destruction (D box) and/or KEN box signals. The spindle assembly checkpoint responds to unattached kinetochores and to kinetochores lacking tension, both of which reflect incomplete biorientation of chromosomes, by delaying the onset of anaphase. It does this by inhibiting Cdc20-APC/C. Certain checkpoint proteins interact directly with Cdc20, but it remains unclear how the checkpoint acts to efficiently inhibit Cdc20-APC/C activity. In the fission yeast, Schizosaccharomyces pombe, we find that the Mad3 and Mad2 spindle checkpoint proteins interact stably with the APC/C in mitosis. Mad3 contains two KEN boxes, conserved from yeast Mad3 to human BubR1, and mutation of either of these abrogates the spindle checkpoint. Strikingly, mutation of the N-terminal KEN box abolishes incorporation of Mad3 into the mitotic checkpoint complex (Mad3-Mad2-Slp1 in S. pombe, where Slp1 is the Cdc20 homolog that we will refer to as Cdc20 hereafter) and stable association of both Mad3 and Mad2 with the APC/C. Our findings demonstrate that this Mad3 KEN box is a critical mediator of Cdc20-APC/C inhibition, without which neither Mad3 nor Mad2 can associate with the APC/C or inhibit anaphase onset.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.