Evidence map›Paper›PMID 26231041›Full record

ArticleeLife2015

Resection is responsible for loss of transcription around a double-strand break in Saccharomyces cerevisiae.

Nicola Manfrini, Michela Clerici, Maxime Wery, Chiara Vittoria Colombo, Marc Descrimes, Antonin Morillon, Fabrizio d'Adda di Fagagna, Maria Pia Longhese

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Multiple mechanisms contribute to double-strand break repair at rereplication forks in Drosophila follicle cells.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
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 4 institutions in 2 countries.

Nicola ManfriniDipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy.
Michela ClericiDipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy.
Maxime WeryInstitut Curie, Dynamics of Genetic Information: Fundamental Basis and Cancer, Université Pierre et Marie Curie, Paris, France.
Chiara Vittoria ColomboDipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy.
Marc DescrimesInstitut Curie, Dynamics of Genetic Information: Fundamental Basis and Cancer, Université Pierre et Marie Curie, Paris, France.
Antonin MorillonInstitut Curie, Dynamics of Genetic Information: Fundamental Basis and Cancer, Université Pierre et Marie Curie, Paris, France.
Fabrizio d'Adda di FagagnaIFOM Foundation, FIRC Institute of Molecular Oncology Foundation, Milan, Italy.
Maria Pia LongheseDipartimento di Biotecnologie e Bioscienze, Università di Milano-Bicocca, Milan, Italy.
University of Milano-Bicocca · ITInstitut Curie · FRDynamique de l'information génétique : bases fondamentales et cancer · FRNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence indicate that the mammalian checkpoint kinase ATM induces transcriptional silencing in cis to DNA double-strand breaks (DSBs) through a poorly understood mechanism. Here we show that in Saccharomyces cerevisiae a single DSB causes transcriptional inhibition of proximal genes independently of Tel1/ATM and Mec1/ATR. Since the DSB ends undergo nucleolytic degradation (resection) of their 5'-ending strands, we investigated the contribution of resection in this DSB-induced transcriptional inhibition. We discovered that resection-defective mutants fail to stop transcription around a DSB, and the extent of this failure correlates with the severity of the resection defect. Furthermore, Rad9 and generation of γH2A reduce this DSB-induced transcriptional inhibition by counteracting DSB resection. Therefore, the conversion of the DSB ends from double-stranded to single-stranded DNA, which is necessary to initiate DSB repair by homologous recombination, is responsible for loss of transcription around a DSB in S. cerevisiae.

Indexed as

DNA Breaks, Double-StrandedTranscription, GeneticDNA Repair EnzymesSaccharomyces cerevisiaeDNA Repair EnzymeschromosomesDNA double-strand breaksgenesresectionRNA polymeraseS. cerevisiaetranscription

Identifiers

PMID26231041
PMCPMC4541074
OpenAlexW2144503197

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.