ArticleMolecular biology of the cell2013
DNA damage checkpoint and recombinational repair differentially affect the replication stress tolerance of Smc6 mutants.
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Smc5/6 Complex Promotes Rad3Molecular and cellular biology · 2022Article
- SMC5/6: Multifunctional Player in Replication.Genes · 2018Review
- Acute Smc5/6 depletion reveals its primary role in rDNA replication by restraining recombination at fork pausing sites.PLoS genetics · 2018Article
- Incision of damaged DNA in the presence of an impaired Smc5/6 complex imperils genome stability.Nucleic acids research · 2016Article
- Smc5/6 Mediated Sumoylation of the Sgs1-Top3-Rmi1 Complex Promotes Removal of Recombination Intermediates.Cell reports · 2016Article
- MTE1 Functions with MPH1 in Double-Strand Break Repair.Genetics · 2016Article
- Mte1 interacts with Mph1 and promotes crossover recombination and telomere maintenance.Genes & development · 2016Article
- Rtt107 Is a Multi-functional Scaffold Supporting Replication Progression with Partner SUMO and Ubiquitin Ligases.Molecular cell · 2015Article
- Functions and regulation of the multitasking FANCM family of DNA motor proteins.Genes & development · 2015Review
- The Slx4-Dpb11 scaffold complex: coordinating the response to replication fork stalling in S-phase and the subsequent mitosis.Cell cycle (Georgetown, Tex.) · 2015Article
- A versatile scaffold contributes to damage survival via sumoylation and nuclease interactions.Cell reports · 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
5 authors at 2 institutions in 2 countries.
Funding
Abstract
DNA damage checkpoint and recombinational repair are both important for cell survival of replication stress. Because these two processes influence each other, isolation of their respective contributions is challenging. Research in budding yeast shows that removal of the DNA helicase Mph1 improves survival of cells with defective Smc5/6 complex under replication stress. mph1 is known to reduce the levels of recombination intermediates in smc6 mutants. Here, we show that mph1 also hyperactivates the Mec1 checkpoint. We dissect the effects of recombination regulation and checkpoint hyperactivation by altering the checkpoint circuitry to enhance checkpoint signaling without reducing recombination intermediate levels. We show that these approaches, similar to mph1, lead to better survival of smc6 cells upon transient replication stress, likely by ameliorating replication and chromosomal segregation defects. Unlike mph1, however, they do not suppress smc6 sensitivity to chronic stress. Conversely, reducing the checkpoint response does not impair survival of smc6 mph1 mutants under chronic stress. These results suggest a two-phase model in which smc6 mutant survival upon transient replication stress can be improved by enhancing Mec1 checkpoint signaling, whereas smc6 sensitivity to chronic stress can be overcome by reducing recombination intermediates.
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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.