ReviewDNA repair2009
DNA end resection: many nucleases make light work.
Review in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
241 citing papers in PubMed, 437 citations in OpenAlex.
- The histone chaperone CAF-1 prevents homologous recombination-mediated instability of the budding yeast ribosomal DNA during replication-coupled DNA double-strand break repair.Nucleic acids research · 2025Article
- Structure-informed evolutionary analysis of the meiotic recombination machinery.bioRxiv : the preprint server for biology · 2025Article
- Re-establishment of H3K9me2 eliminates the transcriptional inhibition of ST18 on meiotic genes and orchestrates female germ cell development.Nucleic acids research · 2025Article
- Transcription near arrested DNA replication forks triggers ribosomal DNA copy number changes.Nucleic acids research · 2025Article
- Checkpoint and recombination pathways independently suppress rates of spontaneous homology-directed chromosomal translocations in budding yeast.Frontiers in genetics · 2025Article
- MRE11 orchestrates porcine oocyte meiotic progression by modulating the spindle assembly checkpoint.Frontiers in cell and developmental biology · 2025Article
- MRE11 is essential for the long-term viability of undifferentiated spermatogonia.Cell proliferation · 2024Article
- Observing one-divalent-metal-ion-dependent and histidine-promoted His-Me family I-PpoI nuclease catalysiseLife · 2024Article
- Observing one-divalent-metal-ion dependent and histidine-promoted His-Me family I-PpoI nuclease catalysis in crystallo.bioRxiv : the preprint server for biology · 2024Article
- Multi-step control of homologous recombination via Mec1/ATR suppresses chromosomal rearrangements.The EMBO journal · 2024Article
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- Meiotic DNA break resection and recombination rely on chromatin remodeler Fun30.bioRxiv : the preprint server for biology · 2024Article
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- A Method for Physical Analysis of Recombination Intermediates in Saccharomyces cerevisiae.Journal of microbiology (Seoul, Korea) · 2023Article
- Review
- DEtail-seq is an ultra-efficient and convenient method for meiotic DNA break profiling in multiple organisms.Science China. Life sciences · 2023Article
- Cdc14 phosphatase counteracts Cdk-dependent Dna2 phosphorylation to inhibit resection during recombinational DNA repair.Nature communications · 2023Article
- Article
- Discrete RNA-DNA hybrid cleavage by the EXD2 exonuclease pinpoints two rate-limiting steps.The EMBO journal · 2023Article
181 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Double-strand breaks (DSBs) are deleterious DNA lesions and if left unrepaired result in severe genomic instability. Cells use two main pathways to repair DSBs: homologous recombination (HR) or non-homologous end joining (NHEJ) depending on the phase of the cell cycle and the nature of the DSB ends. A key step where pathway choice is exerted is in the 'licensing' of 5'-3' resection of the ends to produce recombinogenic 3' single-stranded tails. These tails are substrate for binding by Rad51 to initiate pairing and strand invasion with homologous duplex DNA. Moreover, the single-stranded DNA generated after end processing is important to activate the DNA damage response. The mechanism of end processing is the focus of this review and we will describe recent findings that shed light on this important initiating step for HR. The conserved MRX/MRN complex appears to be a major regulator of DNA end processing. Sae2/CtIP functions with the MRX complex, either to activate the Mre11 nuclease or via the intrinsic endonuclease, in an initial step to trim the DSB ends. In a second step, redundant systems remove long tracts of DNA to reveal extensive 3' single-stranded tails. One system is dependent on the helicase Sgs1 and the nuclease Dna2, and the other on the 5'-3' exonuclease Exo1.
Indexed as
Identifiers
What OpenQuestion holds
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.