ArticlePloS one2012
The Mph1 helicase can promote telomere uncapping and premature senescence in budding yeast.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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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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Who cites it
30 citing papers in PubMed, 33 citations in OpenAlex.
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Break-induced replication is enhanced by a phospho-activated RPA-binding module in Pol32.Nature communications · 2026Article
- Repair of mismatched templates during Rad51-dependent Break-Induced Replication.PLoS genetics · 2022Article
- Mechanisms restraining break-induced replication at two-ended DNA double-strand breaks.The EMBO journal · 2021Article
- Interstitial telomere sequences disrupt break-induced replication and drive formation of ectopic telomeres.Nucleic acids research · 2020Article
- Review
- FANCM suppresses DNA replication stress at ALT telomeres by disrupting TERRA R-loops.Scientific reports · 2019Article
- Moving forward one step back at a time: reversibility during homologous recombination.Current genetics · 2019Review
- DNA Polymerase Delta Synthesizes Both Strands during Break-Induced Replication.Molecular cell · 2019Article
- The FANCM-BLM-TOP3A-RMI complex suppresses alternative lengthening of telomeres (ALT).Nature communications · 2019Article
- FANCM limits ALT activity by restricting telomeric replication stress induced by deregulated BLM and R-loops.Nature communications · 2019Article
- Esc2 promotes telomere stability in response to DNA replication stress.Nucleic acids research · 2019Article
- Dynamic Processing of Displacement Loops during Recombinational DNA Repair.Molecular cell · 2019Article
- Review
- The Smc5/6 complex regulates the yeast Mph1 helicase at RNA-DNA hybrid-mediated DNA damage.PLoS genetics · 2017Article
- FANCM, BRCA1, and BLM cooperatively resolve the replication stress at the ALT telomeres.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Avoidance of APOBEC3B-induced mutation by error-free lesion bypass.Nucleic acids research · 2017Article
- Homology Requirements and Competition between Gene Conversion and Break-Induced Replication during Double-Strand Break Repair.Molecular cell · 2017Article
- RPA Stabilization of Single-Stranded DNA Is Critical for Break-Induced Replication.Cell reports · 2016Article
- Functional characterisation of long intergenic non-coding RNAs through genetic interaction profiling in Saccharomyces cerevisiae.BMC biology · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double strand breaks (DSBs) can be repaired via either Non-Homologous End Joining (NHEJ) or Homology directed Repair (HR). Telomeres, which resemble DSBs, are refractory to repair events in order to prevent chromosome end fusions and genomic instability. In some rare instances telomeres engage in Break-Induced Replication (BIR), a type of HR, in order to maintain telomere length in the absence of the enzyme telomerase. Here we have investigated how the yeast helicase, Mph1, affects DNA repair at both DSBs and telomeres. We have found that overexpressed Mph1 strongly inhibits BIR at internal DSBs however allows it to proceed at telomeres. Furthermore, while overexpressed Mph1 potently inhibits NHEJ at telomeres it has no effect on NHEJ at DSBs within the chromosome. At telomeres Mph1 is able to promote telomere uncapping and the accumulation of ssDNA, which results in premature senescence in the absence of telomerase. We propose that Mph1 is able to direct repair towards HR (thereby inhibiting NHEJ) at telomeres by remodeling them into a nuclease-sensitive structure, which promotes the accumulation of a recombinogenic ssDNA intermediate. We thus put forward that Mph1 is a double-edge sword at the telomere, it prevents NHEJ, but promotes senescence in cells with dysfunctional telomeres by increasing the levels of ssDNA.
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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.