Evidence map›Paper›PMID 25417108›Full record

ArticleCell2014

Dicer promotes transcription termination at sites of replication stress to maintain genome stability.

Stephane E Castel, Jie Ren, Sonali Bhattacharjee, An-Yun Chang, Mar Sánchez, Alberto Valbuena, Francisco Antequera, Robert A Martienssen

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

74 citing papers in PubMed, 115 citations in OpenAlex.

  1. Review
  2. Article
  3. RiboCop surveils pre-rRNA processing by Dicer in cellular quiescence.bioRxiv : the preprint server for biology · 2025
    Article
  4. Review
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  18. Article
  19. ETMR: a tumor entity in its infancy.Acta neuropathologica · 2020
    Review
  20. Review

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Stephane E CastelHoward Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Jie RenHoward Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Sonali BhattacharjeeHoward Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
An-Yun ChangHoward Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, NY 11794, USA.
Mar SánchezInstituto de Biología Funcional y Genómica, CSIC/Universidad de Salamanca, Salamanca 37007, Spain.
Alberto ValbuenaInstituto de Biología Funcional y Genómica, CSIC/Universidad de Salamanca, Salamanca 37007, Spain.
Francisco AntequeraInstituto de Biología Funcional y Genómica, CSIC/Universidad de Salamanca, Salamanca 37007, Spain.
Robert A MartienssenHoward Hughes Medical Institute-Gordon and Betty Moore Foundation, Watson School of Biological Sciences Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, NY 11794, USA. Electronic address: martiens@cshl.edu.
Howard Hughes Medical Institute · USUniversidad de Salamanca · ES

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
RNAi, Histone Modification and the DDB1/CPSF-Like Complex Rik1R01GM076396 · NIGMS · COLD SPRING HARBOR LABORATORY · PI MARTIENSSEN, ROBERT A · 2007 to 2020
$4.9M
Howard Hughes Medical InstituteNCI NIH HHS 5PP30CA045508NCI NIH HHS P30 CA045508NIGMS NIH HHS GM076396NIGMS NIH HHS R01 GM076396
6 · The paper itself

Abstract

Nuclear RNAi is an important regulator of transcription and epigenetic modification, but the underlying mechanisms remain elusive. Using a genome-wide approach in the fission yeast S. pombe, we have found that Dcr1, but not other components of the canonical RNAi pathway, promotes the release of Pol II from the 3? end of highly transcribed genes, and, surprisingly, from antisense transcription of rRNA and tRNA genes, which are normally transcribed by Pol I and Pol III. These Dcr1-terminated loci correspond to sites of replication stress and DNA damage, likely resulting from transcription-replication collisions. At the rDNA loci, release of Pol II facilitates DNA replication and prevents homologous recombination, which would otherwise lead to loss of rDNA repeats especially during meiosis. Our results reveal a novel role for Dcr1-mediated transcription termination in genome maintenance and may account for widespread regulation of genome stability by nuclear RNAi in higher eukaryotes.

Indexed as

DNA ReplicationGenomic InstabilityTranscription Termination, GeneticDNA, AntisenseEndoribonucleasesRNA InterferenceRNA Polymerase IISchizosaccharomycesSchizosaccharomyces pombe ProteinsTranscription, GeneticDcr1 protein, S pombeDNA, AntisenseEndoribonucleasesRNA Polymerase IISchizosaccharomyces pombe Proteins

Identifiers

PMID25417108
PMCPMC4243041
OpenAlexW1974126704

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.