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TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability
DNA anaphase bridges are a potential source of genome instability that may lead to chromosome breakage or nondisjunction during mitosis. Two classes of anaphase bridges can be distinguished: DAPI-positive chromatin bridges and DAPI-negative ultrafine DNA bridges (UFBs). Here, we establish budding ye...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3882784/ https://www.ncbi.nlm.nih.gov/pubmed/24379413 http://dx.doi.org/10.1083/jcb.201305157 |
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author | Germann, Susanne M. Schramke, Vera Pedersen, Rune Troelsgaard Gallina, Irene Eckert-Boulet, Nadine Oestergaard, Vibe H. Lisby, Michael |
author_facet | Germann, Susanne M. Schramke, Vera Pedersen, Rune Troelsgaard Gallina, Irene Eckert-Boulet, Nadine Oestergaard, Vibe H. Lisby, Michael |
author_sort | Germann, Susanne M. |
collection | PubMed |
description | DNA anaphase bridges are a potential source of genome instability that may lead to chromosome breakage or nondisjunction during mitosis. Two classes of anaphase bridges can be distinguished: DAPI-positive chromatin bridges and DAPI-negative ultrafine DNA bridges (UFBs). Here, we establish budding yeast Saccharomyces cerevisiae and the avian DT40 cell line as model systems for studying DNA anaphase bridges and show that TopBP1/Dpb11 plays an evolutionarily conserved role in their metabolism. Together with the single-stranded DNA binding protein RPA, TopBP1/Dpb11 binds to UFBs, and depletion of TopBP1/Dpb11 led to an accumulation of chromatin bridges. Importantly, the NoCut checkpoint that delays progression from anaphase to abscission in yeast was activated by both UFBs and chromatin bridges independently of Dpb11, and disruption of the NoCut checkpoint in Dpb11-depleted cells led to genome instability. In conclusion, we propose that TopBP1/Dpb11 prevents accumulation of anaphase bridges via stimulation of the Mec1/ATR kinase and suppression of homologous recombination. |
format | Online Article Text |
id | pubmed-3882784 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-38827842014-07-06 TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability Germann, Susanne M. Schramke, Vera Pedersen, Rune Troelsgaard Gallina, Irene Eckert-Boulet, Nadine Oestergaard, Vibe H. Lisby, Michael J Cell Biol Research Articles DNA anaphase bridges are a potential source of genome instability that may lead to chromosome breakage or nondisjunction during mitosis. Two classes of anaphase bridges can be distinguished: DAPI-positive chromatin bridges and DAPI-negative ultrafine DNA bridges (UFBs). Here, we establish budding yeast Saccharomyces cerevisiae and the avian DT40 cell line as model systems for studying DNA anaphase bridges and show that TopBP1/Dpb11 plays an evolutionarily conserved role in their metabolism. Together with the single-stranded DNA binding protein RPA, TopBP1/Dpb11 binds to UFBs, and depletion of TopBP1/Dpb11 led to an accumulation of chromatin bridges. Importantly, the NoCut checkpoint that delays progression from anaphase to abscission in yeast was activated by both UFBs and chromatin bridges independently of Dpb11, and disruption of the NoCut checkpoint in Dpb11-depleted cells led to genome instability. In conclusion, we propose that TopBP1/Dpb11 prevents accumulation of anaphase bridges via stimulation of the Mec1/ATR kinase and suppression of homologous recombination. The Rockefeller University Press 2014-01-06 /pmc/articles/PMC3882784/ /pubmed/24379413 http://dx.doi.org/10.1083/jcb.201305157 Text en © 2014 Germann et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Research Articles Germann, Susanne M. Schramke, Vera Pedersen, Rune Troelsgaard Gallina, Irene Eckert-Boulet, Nadine Oestergaard, Vibe H. Lisby, Michael TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title | TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title_full | TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title_fullStr | TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title_full_unstemmed | TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title_short | TopBP1/Dpb11 binds DNA anaphase bridges to prevent genome instability |
title_sort | topbp1/dpb11 binds dna anaphase bridges to prevent genome instability |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3882784/ https://www.ncbi.nlm.nih.gov/pubmed/24379413 http://dx.doi.org/10.1083/jcb.201305157 |
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