ArticlePLoS genetics2012
Topoisomerase II- and condensin-dependent breakage of MEC1ATR-sensitive fragile sites occurs independently of spindle tension, anaphase, or cytokinesis.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Condensin II interacts with BLM helicase in S phase to maintain genome stability.Communications biology · 2025Article
- Dicentric chromosomes are resolved through breakage and repair at their centromeres.Chromosoma · 2024Article
- Topoisomerase II deficiency leads to a postreplicative structural shift in all Saccharomyces cerevisiae chromosomes.Scientific reports · 2021Article
- ATR is essential for preservation of cell mechanics and nuclear integrity during interstitial migration.Nature communications · 2020Article
- Common Fragile Sites Are Characterized by Faulty Condensin Loading after Replication Stress.Cell reports · 2020Article
- Article
- S-phase checkpoint regulations that preserve replication and chromosome integrity upon dNTP depletion.Cellular and molecular life sciences : CMLS · 2017Review
- Not all roads lead to Cdk1.Cell cycle (Georgetown, Tex.) · 2017Article
- Review
- MIIP haploinsufficiency induces chromosomal instability and promotes tumour progression in colorectal cancer.The Journal of pathology · 2017Article
- A Checkpoint-Related Function of the MCM Replicative Helicase Is Required to Avert Accumulation of RNA:DNA Hybrids during S-phase and Ensuing DSBs during G2/M.PLoS genetics · 2016Article
- S phase block following MEC1ATR inactivation occurs without severe dNTP depletion.Biology open · 2015Article
- Chromosome Dynamics during Mitosis.Cold Spring Harbor perspectives in biology · 2015Review
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- Article
- Mechanisms of chromosomal instability in melanoma.Environmental and molecular mutagenesis · 2014Article
- Recombinogenic conditions influence partner choice in spontaneous mitotic recombination.PLoS genetics · 2013Article
- Impediments to replication fork movement: stabilisation, reactivation and genome instability.Chromosoma · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Fragile sites are loci of recurrent chromosome breakage in the genome. They are found in organisms ranging from bacteria to humans and are implicated in genome instability, evolution, and cancer. In budding yeast, inactivation of Mec1, a homolog of mammalian ATR, leads to chromosome breakage at fragile sites referred to as replication slow zones (RSZs). RSZs are proposed to be homologous to mammalian common fragile sites (CFSs) whose stability is regulated by ATR. Perturbation during S phase, leading to elevated levels of stalled replication forks, is necessary but not sufficient for chromosome breakage at RSZs or CFSs. To address the nature of additional event(s) required for the break formation, we examined involvement of the currently known or implicated mechanisms of endogenous chromosome breakage, including errors in replication fork restart, premature mitotic chromosome condensation, spindle tension, anaphase, and cytokinesis. Results revealed that chromosome breakage at RSZs is independent of the RAD52 epistasis group genes and of TOP3, SGS1, SRS2, MMS4, or MUS81, indicating that homologous recombination and other recombination-related processes associated with replication fork restart are unlikely to be involved. We also found spindle force, anaphase, or cytokinesis to be dispensable. RSZ breakage, however, required genes encoding condensin subunits (YCG1, YSC4) and topoisomerase II (TOP2). We propose that chromosome break formation at RSZs following Mec1 inactivation, a model for mammalian fragile site breakage, is mediated by internal chromosomal stress generated during mitotic chromosome condensation.
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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.