ArticleGenes & development2010
De novo telomere formation is suppressed by the Mec1-dependent inhibition of Cdc13 accumulation at DNA breaks.
Article in Genes & development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 87 citations in OpenAlex.
- A CRISPR/Cas9-induced blunt-end telomere system in S. pombe reveals RNase H2-dependent RNA primer removal at the terminal Okazaki fragment of lagging telomeres.Nucleic acids research · 2026Article
- CST complex promotes second-strand synthesis in break-induced replication.Nature structural & molecular biology · 2026Article
- The CST complex mediates a post-resection non-homologous end joining repair pathway and promotes local deletions in Saccharomyces cerevisiae.Cell genomics · 2025Article
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- Hotspot of de novo telomere addition stabilizes linear amplicons in yeast grown in sulfate-limiting conditions.Genetics · 2023Article
- Widely spaced and divergent inverted repeats become a potent source of chromosomal rearrangements in long single-stranded DNA regions.Nucleic acids research · 2023Article
- Deletion of MEC1 suppresses the replicative senescence of the cdc13-2 mutant in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2023Article
- Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022Review
- Telomeres and Cancer.Life (Basel, Switzerland) · 2021Review
- Telomerase subunit Est2 marks internal sites that are prone to accumulate DNA damage.BMC biology · 2021Article
- When the Ends Justify the Means: Regulation of Telomere Addition at Double-Strand Breaks in Yeast.Frontiers in cell and developmental biology · 2021Review
- Emerging non-canonical roles for the Rad51-Rad52 interaction in response to double-strand breaks in yeast.Current genetics · 2020Review
- Functional roles of protein phosphatase 4 in multiple aspects of cellular physiology: a friend and a foe.BMB reports · 2020Review
- Review
- Interaction of yeast Rad51 and Rad52 relieves Rad52-mediated inhibition of de novo telomere addition.PLoS genetics · 2020Article
- Telomere-binding proteins Taz1 and Rap1 regulate DSB repair and suppress gross chromosomal rearrangements in fission yeast.PLoS genetics · 2019Article
- Ser/Thr protein phosphatases in fungi: structure, regulation and function.Microbial cell (Graz, Austria) · 2019Review
- Clathrin Adaptor Complex-interacting Protein Irc6 Functions through the Conserved C-Terminal Domain.Scientific reports · 2019Article
- Fine tuning the level of the Cdc13 telomere-capping protein for maximal chromosome stability performance.Current genetics · 2019Review
- Separable roles for Mec1/ATR in genome maintenance, DNA replication, and checkpoint signaling.Genes & development · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA double-strand breaks (DSBs) are a threat to cell survival and genome integrity. In addition to canonical DNA repair systems, DSBs can be converted to telomeres by telomerase. This process, herein termed telomere healing, endangers genome stability, since it usually results in chromosome arm loss. Therefore, cells possess mechanisms that prevent the untimely action of telomerase on DSBs. Here we report that Mec1, the ATR ortholog, couples the detection of DNA ends with the inhibition of telomerase. Mec1 inhibits telomere healing by phosphorylating Cdc13 on its S306 residue, a phosphorylation event that suppresses Cdc13 accumulation at DSBs. Conversely, telomere addition at accidental breaks is promoted by Pph3, the yeast protein phosphatase 4 (PP4). Pph3 is itself modulated by Rrd1, an activator of PP2A family phosphatases. Rrd1 and Pph3 oppose Cdc13 S306 phosphorylation and are necessary for the efficient accumulation of Cdc13 at DNA breaks. These studies therefore identify a mechanism by which the ATR family of kinases enforces genome integrity, and a process that underscores the contribution of Cdc13 to the fate of DNA ends.
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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.