ArticleCurrent biology : CB2018
Distinct Roles of RZZ and Bub1-KNL1 in Mitotic Checkpoint Signaling and Kinetochore Expansion.
Article in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
77 citing papers in PubMed, 124 citations in OpenAlex.
- Structure and function of the outer kinetochore.Nature reviews. Molecular cell biology · 2026Review
- Kinetochore clustering is mediated by Mps1 phosphorylation of conserved MELT motifs in Stu1.The Journal of cell biology · 2026Article
- hSpindly dynamics modulate spindle assembly checkpoint signaling, promoting resistance to mitotic inhibitors.iScience · 2026Article
- Fidelity-Ensuring Consistency of Mitosis is Safeguarded by the 53BP1-USP28-p53 Pathway.bioRxiv : the preprint server for biology · 2026Article
- The kinetochore corona orchestrates chromosome congression through transient microtubule interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Kinetochore clustering is mediated by Mps1 phosphorylation of conserved MELT motifs in Stu1.bioRxiv : the preprint server for biology · 2026Article
- Linking kinetochore attachment to checkpoint control: the role of Aurora B in BubR1 acetylation.Nucleic acids research · 2026Article
- KIF18A promotes chromosome congression in cooperation with CENP-E downstream of CENP-C.Cell reports · 2025Article
- The BUB1 and BUBR1 paralogs scaffold the kinetochore fibrous corona.Science advances · 2025Article
- CENcyclopedia: dynamic landscape of kinetochore architecture throughout the cell cycle.Nature communications · 2025Article
- Dynamic phosphorylation of MIS12 ensures accurate kinetochore-microtubule attachment by expanding the fibrous corona.Molecular biology of the cell · 2025Article
- CRISPR GENome and epigenome engineering improves loss-of-function genetic-screening approaches.Cell reports methods · 2025Article
- Interplay of kinetochores and catalysts drives rapid assembly of the mitotic checkpoint complex.Nature communications · 2025Article
- Article
- Fibrous corona is reduced in cancer cell lines that attenuate microtubule nucleation from kinetochores.Cancer science · 2025Article
- ZW10: an emerging orchestrator of organelle dynamics during the cell division cycle.Journal of molecular cell biology · 2024Review
- Mosaic variegated aneuploidy in development, ageing and cancer.Nature reviews. Genetics · 2024Review
- Escaping from CRISPR-Cas-mediated knockout: the facts, mechanisms, and applications.Cellular & molecular biology letters · 2024Review
- A conserved CENP-E region mediates BubR1-independent recruitment to the outer corona at mitotic onset.Current biology : CB · 2024Article
- A farnesyl-dependent structural role for CENP-E in expansion of the fibrous corona.The Journal of cell biology · 2024Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
The Mad1-Mad2 heterodimer is the catalytic hub of the spindle assembly checkpoint (SAC), which controls M phase progression through a multi-subunit anaphase inhibitor, the mitotic checkpoint complex (MCC) [1, 2]. During interphase, Mad1-Mad2 generates MCC at nuclear pores [3]. After nuclear envelope breakdown (NEBD), kinetochore-associated Mad1-Mad2 catalyzes MCC assembly until all chromosomes achieve bipolar attachment [1, 2]. Mad1-Mad2 and other factors are also incorporated into the fibrous corona, a phospho-dependent expansion of the outer kinetochore that precedes microtubule attachment [4-6]. The factor(s) involved in targeting Mad1-Mad2 to kinetochores in higher eukaryotes remain controversial [7-12], and the specific phosphorylation event(s) that trigger corona formation remain elusive [5, 13]. We used genome editing to eliminate Bub1, KNL1, and the Rod-Zw10-Zwilch (RZZ) complex in human cells. We show that RZZ's sole role in SAC activation is to tether Mad1-Mad2 to kinetochores. Separately, Mps1 kinase triggers fibrous corona formation by phosphorylating two N-terminal sites on Rod. In contrast, Bub1 and KNL1 activate kinetochore-bound Mad1-Mad2 to produce a "wait anaphase" signal but are not required for corona formation. We also show that clonal lines isolated after BUB1 disruption recover Bub1 expression and SAC function through nonsense-associated alternative splicing (NAS). Our study reveals a fundamental division of labor in the mammalian SAC and highlights a transcriptional response to nonsense mutations that can reduce or eliminate penetrance in genome editing experiments.
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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.