ArticleMolecular and cellular biology2009
Smc5-Smc6-dependent removal of cohesin from mitotic chromosomes.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Single-cell RNA sequencing in silent corticotroph tumors confirms impaired POMC processing and provides new insights into their invasive behavior.European journal of endocrinology · 2022Article
- Live-cell single-molecule tracking highlights requirements for stable Smc5/6 chromatin association in vivo.eLife · 2021Article
- Generation and Analysis of dsDNA Breaks for Checkpoint and Repair Studies in Fission Yeast.Methods in molecular biology (Clifton, N.J.) · 2021Article
- SMC5/6 acts jointly with Fanconi anemia factors to support DNA repair and genome stability.EMBO reports · 2020Article
- A genome-wide RNAi screen identifies the SMC5/6 complex as a non-redundant regulator of a Topo2a-dependent G2 arrest.Nucleic acids research · 2019Article
- Brc1 Promotes the Focal Accumulation and SUMO Ligase Activity of Smc5-Smc6 during Replication Stress.Molecular and cellular biology · 2019Article
- SMC5/6: Multifunctional Player in Replication.Genes · 2018Review
- Review
- DNA Topoisomerase II modulates acetyl-regulation of cohesin-mediated chromosome dynamics.Current genetics · 2017Article
- Specialized interfaces of Smc5/6 control hinge stability and DNA association.Nature communications · 2017Article
- An acetyltransferase-independent function of Eso1 regulates centromere cohesion.Molecular biology of the cell · 2016Article
- Resolving complex chromosome structures during meiosis: versatile deployment of Smc5/6.Chromosoma · 2016Review
- Chromatin association of the SMC5/6 complex is dependent on binding of its NSE3 subunit to DNA.Nucleic acids research · 2016Article
- NSMCE2 suppresses cancer and aging in mice independently of its SUMO ligase activity.The EMBO journal · 2015Article
- Functional interplay between cohesin and Smc5/6 complexes.Chromosoma · 2014Review
- The chromosomal association of the Smc5/6 complex depends on cohesion and predicts the level of sister chromatid entanglement.PLoS genetics · 2014Article
- Hypomorphism in human NSMCE2 linked to primordial dwarfism and insulin resistance.The Journal of clinical investigation · 2014Article
- The SMC5/6 complex is involved in crucial processes during human spermatogenesis.Biology of reproduction · 2014Article
- H2A.Z-dependent regulation of cohesin dynamics on chromosome arms.Molecular and cellular biology · 2014Article
- Smc5/6-mediated regulation of replication progression contributes to chromosome assembly during mitosis in human cells.Molecular biology of the cell · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The function of the essential cohesin-related Smc5-Smc6 complex has remained elusive, though hypomorphic mutants have defects late in recombination, in checkpoint maintenance, and in chromosome segregation. Recombination and checkpoints are not essential for viability, and Smc5-Smc6-null mutants die in lethal mitoses. This suggests that the chromosome segregation defects may be the source of lethality in irradiated Smc5-Smc6 hypomorphs. We show that in smc6 mutants, following DNA damage in interphase, chromosome arm segregation fails due to an aberrant persistence of cohesin, which is normally removed by the Separase-independent pathway. This postanaphase persistence of cohesin is not dependent on DNA damage, since the synthetic lethality of smc6 hypomorphs with a topoisomerase II mutant, defective in mitotic chromosome structure, is also due to the retention of cohesin on undamaged chromosome arms. In both cases, Separase overexpression bypasses the defect and restores cell viability, showing that defective cohesin removal is a major determinant of the mitotic lethality of Smc5-Smc6 mutants.
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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.