ArticleMolecular and cellular biology2001
Topoisomerase III acts upstream of Rad53p in the S-phase DNA damage checkpoint.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 69 citations in OpenAlex.
- Tolerance to replication stress requires Dun1p kinase and activation of the electron transport chain.Biochimica et biophysica acta. Molecular cell research · 2023Article
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- Review
- Unresolved Recombination Intermediates Cause aGenetics · 2019Article
- The dissolution of double Holliday junctions.Cold Spring Harbor perspectives in biology · 2014Review
- Resolution by unassisted Top3 points to template switch recombination intermediates during DNA replication.The Journal of biological chemistry · 2013Article
- A Rad53 independent function of Rad9 becomes crucial for genome maintenance in the absence of the Recq helicase Sgs1.PloS one · 2013Article
- Distinct roles of Mus81, Yen1, Slx1-Slx4, and Rad1 nucleases in the repair of replication-born double-strand breaks by sister chromatid exchange.Molecular and cellular biology · 2012Article
- Pathways for Holliday junction processing during homologous recombination in Saccharomyces cerevisiae.Molecular and cellular biology · 2011Article
- Holliday junction-containing DNA structures persist in cells lacking Sgs1 or Top3 following exposure to DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Identification of a Functional Type IA Topoisomerase, LdTopIIIβ, from Kinetoplastid Parasite Leishmania donovani.Enzyme research · 2011Article
- The roles of the Saccharomyces cerevisiae RecQ helicase SGS1 in meiotic genome surveillance.PloS one · 2010Article
- TOPO3alpha influences antigenic variation by monitoring expression-site-associated VSG switching in Trypanosoma brucei.PLoS pathogens · 2010Article
- Large-scale expansions of Friedreich's ataxia GAA repeats in yeast.Molecular cell · 2009Article
- Topo IIIalpha and BLM act within the Fanconi anemia pathway in response to DNA-crosslinking agents.Cytogenetic and genome research · 2009Article
- The Arabidopsis BLAP75/Rmi1 homologue plays crucial roles in meiotic double-strand break repair.PLoS genetics · 2008Article
- RecQ helicases: guardian angels of the DNA replication fork.Chromosoma · 2008Review
- The genetic consequences of ablating helicase activity and the Top3 interaction domain of Sgs1.DNA repair · 2008Article
- Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3beta.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Top3 processes recombination intermediates and modulates checkpoint activity after DNA damage.Molecular biology of the cell · 2006Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deletion of the Saccharomyces cerevisiae TOP3 gene, encoding Top3p, leads to a slow-growth phenotype characterized by an accumulation of cells with a late S/G2 content of DNA (S. Gangloff, J. P. McDonald, C. Bendixen, L. Arthur, and R. Rothstein, Mol. Cell. Biol. 14:8391-8398, 1994). We have investigated the function of TOP3 during cell cycle progression and the molecular basis for the cell cycle delay seen in top3Delta strains. We show that top3Delta mutants exhibit a RAD24-dependent delay in the G2 phase, suggesting a possible role for Top3p in the resolution of abnormal DNA structures or DNA damage arising during S phase. Consistent with this notion, top3Delta strains are sensitive to killing by a variety of DNA-damaging agents, including UV light and the alkylating agent methyl methanesulfonate, and are partially defective in the intra-S-phase checkpoint that slows the rate of S-phase progression following exposure to DNA-damaging agents. This S-phase checkpoint defect is associated with a defect in phosphorylation of Rad53p, indicating that, in the absence of Top3p, the efficiency of sensing the existence of DNA damage or signaling to the Rad53 kinase is impaired. Consistent with a role for Top3p specifically during S phase, top3Delta mutants are sensitive to the replication inhibitor hydroxyurea, expression of the TOP3 mRNA is activated in late G1 phase, and DNA damage checkpoints operating outside of S phase are unaffected by deletion of TOP3. All of these phenotypic consequences of loss of Top3p function are at least partially suppressed by deletion of SGS1, the yeast homologue of the human Bloom's and Werner's syndrome genes. These data implicate Top3p and, by inference, Sgs1p in an S-phase-specific role in the cellular response to DNA damage. A model proposing a role for these proteins in S phase is presented.
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