ArticleNucleic acids research2022
Cdc48Ufd1/Npl4 segregase removes mislocalized centromeric histone H3 variant CENP-A from non-centromeric chromatin.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 14 citations in OpenAlex.
- Valosin-containing protein is cargo in Amyloid Precursor Protein extracellular vesicles.Cell communication and signaling : CCS · 2026Article
- Histone Nuclear Import and Beyond: Multifunctional Roles of Importins.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Keeping it centered: decoding the activities that regulate yeast histone H3 variant Cse4 and confine it to centromeres.Frontiers in cell and developmental biology · 2026Review
- The nuclear dynamic of CDC48 is affected during the immune response in plants.Plant signaling & behavior · 2025Article
- Chromatin remodeling activity of EP400 safeguards chromosomal stability by preventing CENP-A mislocalization.Cell reports · 2025Article
- Oncohistone H3 E97K mutation facilitates CENP-A mislocalization and chromosomal instability in budding yeast.Nucleic acids research · 2025Article
- Mck1-mediated proteolysis of CENP-A prevents mislocalization of CENP-A for chromosomal stability in Saccharomyces cerevisiae.Genetics · 2024Article
- Set2 regulates Ccp1 and Swc2 to ensure centromeric stability by retargeting CENP-A.Nucleic acids research · 2024Article
- Cdc48 and its co-factor Ufd1 extract CENP-A from centromeric chromatin and can induce chromosome elimination in the fission yeast Schizosaccharomyces pombe.Biology open · 2024Article
- Interaction of histone H4 with Cse4 facilitates conformational changes in Cse4 for its sumoylation and mislocalization.Nucleic acids research · 2024Article
- β-TrCP-Mediated Proteolysis of Mis18β Prevents Mislocalization of CENP-A and Chromosomal Instability.Molecular and cellular biology · 2024Article
- Identification of crucial inflammaging related risk factors in multiple sclerosis.Frontiers in molecular neuroscience · 2024Article
- The histone H3/H4 chaperone CHAF1B prevents the mislocalization of CENP-A for chromosomal stability.Journal of cell science · 2023Article
- p97/VCP drives turnover of SUMOylated centromeric CCAN proteins and CENP-A.Molecular biology of the cell · 2023Article
- SUMO control of centromere homeostasis.Frontiers in cell and developmental biology · 2023Review
- Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Restricting the localization of CENP-A (Cse4 in Saccharomyces cerevisiae) to centromeres prevents chromosomal instability (CIN). Mislocalization of overexpressed CENP-A to non-centromeric chromatin contributes to CIN in budding and fission yeasts, flies, and humans. Overexpression and mislocalization of CENP-A is observed in cancers and is associated with increased invasiveness. Mechanisms that remove mislocalized CENP-A and target it for degradation have not been defined. Here, we report that Cdc48 and its cofactors Ufd1 and Npl4 facilitate the removal of mislocalized Cse4 from non-centromeric chromatin. Defects in removal of mislocalized Cse4 contribute to lethality of overexpressed Cse4 in cdc48,ufd1 andnpl4 mutants. High levels of polyubiquitinated Cse4 and mislocalization of Cse4 are observed in cdc48-3, ufd1-2 and npl4-1mutants even under normal physiological conditions, thereby defining polyubiquitinated Cse4 as the substrate of the ubiquitin directed segregase Cdc48Ufd1/Npl4. Accordingly, Npl4, the ubiquitin binding receptor, associates with mislocalized Cse4, and this interaction is dependent on Psh1-mediated polyubiquitination of Cse4. In summary, we provide the first evidence for a mechanism that facilitates the removal of polyubiquitinated and mislocalized Cse4 from non-centromeric chromatin. Given the conservation of Cdc48Ufd1/Npl4 in humans, it is likely that defects in such pathways may contribute to CIN in human cancers.
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