ArticleNature cell biology2016
DNA damage signalling targets the kinetochore to promote chromatin mobility.
Article in Nature cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 93 citations in OpenAlex.
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- The Role of Transient Crosslinks in the Chromatin Search Response to DNA Damage.International journal of molecular sciences · 2025Article
- The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery.Cell reports · 2025Article
- Nuclear and genome dynamics underlying DNA double-strand break repair.Nature reviews. Molecular cell biology · 2025Review
- Regulation of Precise DNA Repair by Nuclear Actin Polymerization: A Chance for Improving Gene Therapy?Cells · 2024Review
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- The power of weak, transient interactions across biology: A paradigm of emergent behavior.Physica D. Nonlinear phenomena · 2023Article
- Multi-Scale Imaging of the Dynamic Organization of Chromatin.International journal of molecular sciences · 2023Review
- Double-strand break repair and mis-repair in 3D.DNA repair · 2023Article
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- Uncovering Bleomycin-Induced Genomic Alterations and Underlying Mechanisms in the YeastApplied and environmental microbiology · 2022Article
- Review
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- Coupling DNA Replication and Spindle Function inCells · 2021Review
- Modified chromosome structure caused by phosphomimetic H2A modulates the DNA damage response by increasing chromatin mobility in yeast.Journal of cell science · 2021Article
- Collaborations between chromatin and nuclear architecture to optimize DNA repair fidelity.DNA repair · 2021Review
- Fission yeast condensin contributes to interphase chromatin organization and prevents transcription-coupled DNA damage.Genome biology · 2020Article
- Help or hindrance: how do microtubule-based forces contribute to genome damage and repair?Current genetics · 2020Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In budding yeast, chromatin mobility increases after a DNA double-strand break (DSB). This increase is dependent on Mec1, the yeast ATR kinase, but the targets responsible for this phenomenon are unknown. Here we report that the Mec1-dependent phosphorylation of Cep3, a kinetochore component, is required to stimulate chromatin mobility after DNA breaks. Cep3 phosphorylation counteracts a constraint on chromosome movement imposed by the attachment of centromeres to the spindle pole body. A second constraint, imposed by the tethering of telomeres to the nuclear periphery, is also relieved after chromosome breakage. A non-phosphorylatable Cep3 mutant that impairs DSB-induced chromatin mobility is proficient in DSB repair, suggesting that break-induced chromatin mobility may be dispensable for homology search. Rather, we propose that the relief of centromeric constraint promotes cell cycle arrest and faithful chromosome segregation through the engagement of the spindle assembly checkpoint.
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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.