ArticleOpen biology2020
Topoisomerase IIα prevents ultrafine anaphase bridges by two mechanisms.
Article in Open biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- Article
- Structural evidence for elastic tethers connecting separating chromosomes in crane-fly spermatocytes.Life science alliance · 2023Article
- Processing DNA lesions during mitosis to prevent genomic instability.Biochemical Society transactions · 2022Review
- CDK4/6 inhibitors induce replication stress to cause long-term cell cycle withdrawal.The EMBO journal · 2022Article
- The Role of DNA Topoisomerase Binding Protein 1 (TopBP1) in Genome Stability inPlants (Basel, Switzerland) · 2021Article
- Regulation of mitotic chromosome architecture and resolution of ultrafine anaphase bridges by PICH.Cell cycle (Georgetown, Tex.) · 2021Article
- Increased numbers of nucleoli in a genome-wide RNAi screen reveal proteins that link the cell cycle to RNA polymerase I transcription.Molecular biology of the cell · 2021Article
- CENP-A chromatin prevents replication stress at centromeres to avoid structural aneuploidy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- DNA-Binding Anticancer Drugs: One Target, Two Actions.Molecules (Basel, Switzerland) · 2021Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Topoisomerase IIα (Topo IIα), a well-conserved double-stranded DNA (dsDNA)-specific decatenase, processes dsDNA catenanes resulting from DNA replication during mitosis. Topo IIα defects lead to an accumulation of ultrafine anaphase bridges (UFBs), a type of chromosome non-disjunction. Topo IIα has been reported to resolve DNA anaphase threads, possibly accounting for the increase in UFB frequency upon Topo IIα inhibition. We hypothesized that the excess UFBs might also result, at least in part, from an impairment of the prevention of UFB formation by Topo IIα. We found that Topo IIα inhibition promotes UFB formation without affecting the global disappearance of UFBs during mitosis, but leads to an aberrant UFB resolution generating DNA damage within the next G1. Moreover, we demonstrated that Topo IIα inhibition promotes the formation of two types of UFBs depending on cell cycle phase. Topo IIα inhibition during S-phase compromises complete DNA replication, leading to the formation of UFB-containing unreplicated DNA, whereas Topo IIα inhibition during mitosis impedes DNA decatenation at metaphase-anaphase transition, leading to the formation of UFB-containing DNA catenanes. Thus, Topo IIα activity is essential to prevent UFB formation in a cell-cycle-dependent manner and to promote DNA damage-free resolution of UFBs.
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